Effects of glucagon on canine intestinal sodium and water fluxes and regional blood flow.

1. Glucagon (0-05 or 0-5 microng/kg. min) was infused into a mesenteric artery of a canine ileal segment from which transport was measured (direct infusion) or into a mesenteric artery of an adjacent non-perfused segment (indirect infusion). Unidirectional Na and H2O fluxes and arterial and mesenteric vein pressures and total and absorptive site blood flows were measured. 2. Direct glucagon infusion increased the absorptive and secretory fluxes of Na and H2O and absorptive site blood flow, and decreased absorptive site resistance and arterial and mesenteric vein pressure. Indirect glucagon infusion had the opposite effects. 3. Neither the direct arterial infusion of histamine (0-1-53 microng/kg. min) nor the I.V. infusion of glucose (0-2 g/min) or insulin (0-1 micron/kg) or glucose plus insulin, mimicked the effects of glucagon. 4. The unidirectional secretory and absorptive fluxes of both Na and H2O were linearly related to the calculated capillary pressure during glucagon infusion. 5. It was concluded that the effects of glucagon on gut transport were due to effects exerted through the cardiovascular system.     

Effects of hyperoncotic albumin and parathyroid hormone infusion on jejunal electrolyte and water absorption in the rat

Preferential plasma volume expansion by infusion of hyperoncotic albumin solution dialyzed against distilled water (calcium-poor albumin) decreases sodium reabsorption in the dog proximal renal tubule during hydropenia. No such decrease is observed when infusing a calcium-rich hyperoncotic albumin solution. A possible role of parathyroid hormone (PTH) has been postulated. To investigate whether similar changes could be observed in intestinal electrolyte and water absorption, the effects of systemic hyperoncotic albumin infusion on jejunal transport of water, sodium, and calcium were studied in hydropenic rats by perfusing proximal jejunum in situ. It was further sought whether PTH could play a direct role in jejunal electrolyte and water transfer.Following infusion of calcium-poor, sodium-poor hyperoncotic albumin solution (group I), net jejunal absorption of water, sodium, and calcium decreased significantly when compared to control. Concurrently, lumen-to-mucosa (1-m) calcium flux, measured using 45 Ca, diminished significantly. Following infusion of calcium-rich, sodium-poor hyperoncotic albumin solution (group II), no changes in net or unidirectional fluxes were observed. After infusion of calcium-rich, sodium-rich hyperoncotic albumin solution (group III), net jejunal absorption of water and sodium, but not of calcium, were found significantly decreased when compared to control.Plasma ionized calcium increased 10 min after calcium-rich hyperoncotic albumin loading, but decreased significantly at that time when the calcium-poor hyperoncotic albumin solution was infused. However, 30 min after each of the calcium-rich and calcium-poor albumin infusion, plasma ionized calcium was increased in both groups of rats. Plasma immunoreactive PTH was unchanged 30 min after expansion with the calcium-rich solution but it increased significantly after expansion with the calcium-poor solution.Intravenous infusion of bovine PTH (group IV) resulted in a decrease of net jejunal water, sodium, and calcium flux. The decrease in net calcium transport was accompanied by a decrease in 1-m calcium flux. No such changes were observed when PTH was replaced by vehicle (group V).It is concluded that: (1) hyperoncotic albumin infusion induces jejunal water, sodium, and calcium flux changes dependent on the calcium and sodium content of the infused solution: calcium-poor, sodium-poor hyperoncotic albumin infusion leads to a decrease in net jejunal electrolyte and water absorption possibly via stimulation of PTH secretion; (2) sodium-poor hyperoncotic albumin infusion does not modify per se these fluxes in the hydropenic rat; (3) exogenous PTH infusion as well as endogenous stimulation of PTH secretion results in a comparable decrease of jejunal water, sodium, and calcium absorption.     

Canine renal vascular response to hyperoncotic dextran in kidneys with or without glomerular filtration

The effect of intrarenal arterial infusion of hyperoncotic dextran on renal hemodynamics and excretion was studied in anesthetized dogs. To examine the role of glomerular filtration and tubular flow in the hemodynamic response, several kidney models were employed. Nonfiltering kidneys (NFK) were produced by combined ischemia and ureteral obstruction (UO). Additionally, kidneys with only UO and a lack of filtration as well as kidneys with only ischemia and glomerular filtration were studied. Renal blood flow in normal kidneys was increased by hyperoncotic dextran from 357 +/- 47 to 486 +/- 65 ml X min-1 X 100 g-1, with a corresponding decrease in renal vascular resistance. Ischemic kidneys responded likewise to the dextran infusion, increasing renal blood flow from 261 +/- 31 to 339 +/- 29 ml X min-1 X 100 g-1. Glomerular filtration rate was reduced by the dextran infusion from 80.1 +/- 7.9 to 60.7 +/- 6.6 in normal kidneys and from 31.8 +/- 9.6 to 20.2 +/- 5.8 ml X min-1 X 100 g-1 in ischemic kidneys. Urine flow and sodium excretion were also reduced in these kidneys. In contrast, both NFK and UO, which lacked filtration and tubular flow, did not vasodilate in response to dextran. Renal blood flow remained unchanged from control values (NFK: 146 +/- 6, UO: 111 +/- 22 ml X min-1 X 100 g-1) in these kidneys. These experiments show that the renal vascular response to hyperoncotic dextran is not due to a change in blood volume or viscosity nor to a direct pharmacologic action of dextran. The most likely explanation is that hyperoncotic dextran alters tubuloglomerular feedback control of renal vascular resistance by decreasing filtration and altering tubular flow and/or composition. However, the involvement of another intrarenal vasodilatory system cannot be discounted.     

Transport of sodium and secretion of potassium and bicarbonate by the colon of normal and sodium-depleted rats

1. Ascending and descending colonic segments of normal and Na-depleted rats were perfused in vivo with isotonic solutions of varying Na concentration and the unidirectional Na fluxes and secretion rate of K and bicarbonate and the transmucosal electrical p.d. were measured.

2. Potential difference was greater in Na-depleted rats, especially towards the distal end of the descending colon. With reduction of luminal Na concentration, p.d. was reduced.

3. The ascending and descending segments were similar in regard to Na transport except that the latter had lower passive permeability. Na depletion caused an increase of Na influx rate, Na net flux rate and Na exchange diffusion whilst the mucosal passive Na permeability decreased. These changes resulted in a reduction in the critical luminal Na concentration, i.e. the concentration at which the unidirectional fluxes were equal.

4. K secretion rate was similar in the ascending and descending colon and was increased by Na depletion. In all rats, it was reduced when the luminal Na concentration was low.

5. Bicarbonate secretion rate was unaffected by the Na depletion and all solutions remained isotonic during perfusion.

6. The results confirmed that active Na transport was stimulated by Na depletion but indicated that this was probably not the only factor in the elevation of transmucosal p.d.

     

Effect of feeding a high protein diet on solute-coupled water absorption from rat colon

Using an in vivo sac technique, net transport of water, Na, Cl and K was studied in the colon ascendens of rats fed either a high carbohydrate (HC) or high protein (HP) diet, since water intake is elevated in HP-rats. The ligated colon sacs were filled with isotonic Krebs-Henseleit solution.Net Na and Cl absorption rates related to 1 g intestinal dry weight were 46% and 30% higher in HP-rats compared with HC-rats. Net water absorption in HP-rats exceeded that in HC-rats by 115%. Therefore the ratio between net water absorption and net absorption of solutes was higher in HP-rats than in HC-rats, and thus the hypertonicity of the absorbate was lower in the HP-rats. There was a net secretion of K in both groups of rats to about the same extent.Experiments with²²Na indicate that the increased net Na absorption in HP-rats was due to an increased unidirectional Na transport from the lumen to the blood side of the colon.The group difference in the ratio between net absorption of water and solutes might be a manifestation of regulatory mechanism controlling intestinal water absorption.Supported by the Deutsche Forschungsgemeinschaft     

Effects of acute maternal hyperglycaemia and hyperosmolality on maternofetal transfer of calcium and magnesium across the in situ perfused rat placenta.

The effects of acute maternal hyperglycaemia and hyperosmolality on maternofetal placental transfer of Ca, Mg and 51Cr-EDTA were investigated in the rat. On day 21 of gestation (term = 23 d) the fetal circulation of the in situ placenta of anaesthetised rats was perfused with a Mg-free Krebs Ringer solution and the unidirectional maternofetal fluxes of Ca (CaJmf) and Mg (MgJmf), and the unidirectional maternofetal clearance of 51Cr-EDTA ((EDTA)Kmf) were determined before and during maternal hyperglycaemia, hyperosmolality and volume expansion, attained by infusing 30% D-glucose, 25% mannitol and 0.9% saline solutions, respectively, into the maternal circulation. MgJmf was significantly reduced during glucose infusion (23.9 +/- 1.2 v 28.2 +/- 1.4 nmol min(-1) g(-1) placenta during control perfusion (mean +/- SEM); p < 0.005) and during mannitol infusion (28.2 +/- 1.0 v 33.5 +/- 1.5 nmol min(-1) g(-1) placenta; p < 0.001). CaJmf and (EDTA)Kmf were not significantly altered by maternal hyperglycaemia or hyperosmolality. There was no significant change in MgJmf during infusion of saline into the maternal circulation. Maternal plasma Na concentration was significantly reduced in both glucose and mannitol infusion experiments, whereas maternal plasma Mg concentration was significantly reduced only during glucose infusion. We postulate that the reduced maternal plasma Na concentration in the glucose and mannitol experiments might decrease MgJmf via alteration of placental Na+/Mg2+ exchange activity.     

Villous tissue osmolality and intestinal transport of water and electrolytes

The villous tissue hyperosmolality created by the intestinal countercurrent multiplier has been proposed to be of importance for fluid transport across the intestinal epithelium in vivo. This study was performed to test this hypothesis. Net transport of fluid and electrolytes (sodium, potassium and chloride), as well as unidirectional fluxes of water and sodium were determined in the small intestine of the cat. The villous osmolality was altered by varying the composition of sodium and glucose in the isotonic solutions perfusing the intestinal lumen. Net transport of fluid was correlated to tissue osmolality mainly due to an increase of the unidirectional flux of water from lumen to tissue with augmented tissue osmolality. The results are thus consistent with the view that the intestinal countercurrent multiplier is of essential importance for net water transport. A correlation was found between net water and net sodium intestinal transport. A similar correlation was also demonstrated between net sodium and net chloride absorption rates in the jejunum while in the ileum net loss of sodium into the intestinal lumen was not accompanied by any corresponding loss of chloride ions. This observation suggests the presence of a sodium independent transport mechanism for chloride in the ilium but not in the jejunum.     

Influence of ammonia on sodium absorption in rat proximal colon

The influence of ammonia on sodium and chloride fluxes in rat proximal colon was studied in Ussing chamber experiments. Under short-circuit conditions, the proximal colon absorbed sodium and secreted chloride. The presence of ammonia (30 mmol 1(-1) mucosal) diminished Na+ absorption, but had hardly any influence on Cl- fluxes. Blocking the apical Na+/H+ exchanger isoform NHE2 by amiloride or HOE642 diminished absorptive Na+ and Cl- fluxes. In contrast, the NHE3-specific antagonist S3226 was ineffective. Amiloride and HOE642 also inhibited the effect of ammonia on net sodium absorption. In bicarbonate-free buffer solution, ammonia failed to alter the absorptive fluxes of sodium and chloride, but increased the secretory fluxes of Na+ and Cl-. The latter effect was blocked by HOE642. These results suggest that basal NaCl absorption in rat proximal colon depends to a large extent on NHE2. Mucosal ammonium decreases Na+ absorption and this effect can be antagonized by blocking NHE2. This observation suggests that ammonium interacts with the apical Na+/H+ exchanger, thereby diminishing sodium absorption.     

Cation transport and regulatory volume increase in red blood cells of northern fur seals (Callorhinus ursinus)

We investigated the membrane transport of Na and K ions in red blood cells (RBCs) of northern fur seal (Callorhinus ursinus) by measurement of unidirectional fluxes. Like red blood cells of other carnivores, those of northern fur seal contain high Na and low K concentrations, which result from the lack of Na–K ATPase activity on their membranes. In physiological conditions, activities of bumetanide-sensitive Na, K–Cl cotransport and amiloride-sensitive Na/H exchange were measured. K–Cl cotransport and Na–Cl cotransport were not detected. Hypertonicity activated only Na/H exchange. We further examined the ion transport systems for regulatory volume increase (RVI) in red blood cells. In the hyperosmotic condition, shrunken RBCs restored their original cell volume in Na medium but not in Na-free medium, and this restoration with Na medium was inhibited by amiloride. From these results, it is suggested that RVI in northern fur seal RBCs are performed by amiloride-sensitive Na/H exchanger but not Na, K–Cl cotransporter. H. Fujise is deceased.     

Lymph capillary pressure of rat intestinal villi during fluid absorption.

A newly developed intestinal preparation is described for determining lymph capillary pressure (PL) in the villi in vivo and in vitro. Determination of PL provided an estimate of tissue fluid pressure in the villi. PL was related to the fluid absorption rate and increased by lymphatic obstruction. During fluid absorption from isotonic mucosal fluid, PL was 1.4 +/- 0.5 or 1.1 +/- 0.4 cmH2O determined in vivo or in vitro, respectively. Both pressures were essentially in the same range as that (0.7 +/- 0.3--1.3 +/- 0.5 cmH2O) in which the mucosal fluid was isotonic Na2SO4 solution or Na-free solutions from which little fluid absorption occurred. This range of pressures may be taken as the normal tissue fluid pressure in the villi. At a high rate of fluid absorption from hypotonic mucosal fluid, PL increased to 5.2 +/- 1.4 cmH2O and tissue fluid pressure was also similarly increased. It is concluded that the fluid absorptive process by the epithelium could not develop an appreciable hydrostatic pressure in the villus tissue space or in the lymphatics.     

不同晶体液对胃肠道手术婴儿电解质、血糖的影响

目的 比较生理盐水、2.5%葡萄糖生理盐水及复方电解质液对婴儿胃肠道手术电解质、血糖的影响,探讨婴儿的胃肠道手术输入何种液体更为合适。方法 选择我院行胃肠道手术的婴儿60例,随机分为等张的生理盐水组（C组）,1/2张2.5%葡萄糖生理盐水组（G组）及等张的复方电解质液组（F组）3组,每组20例。手术期间各组患儿的输液按各实验分组的方案进行。各组患儿均于静脉输液前（T0）、静脉输液30 min（T1）、静脉输液60 min（T2）、静脉输液90 min（T3）及静脉输液120 min（T4）时记录HR及MAP的变化;并在上述各时间点抽取桡动脉血测血Na+、Cl-、K+、Glu;术后2 h（T5）再抽血测定一次Glu（术后2 h内仍输注围术期的同种液体）。结果 与T0时比较,T3、T4时G组Na+、K+值降低（P＜0.05）;T4时G组Cl-值降低（P＜0.05）;T2、T3、T4时C组Cl-值升高（P＜0.05）;T2、T3、T4时C组与F组的Glu值升高（P＜0.05）;T5时C组与F组的Glu值降低（P＜0.05）;而T1、T2、T3、T4、T5时G组的Glu值持续升高（P＜0.05）。与C组比较,T2、T3、T4时G组Na+值、G组和F组Cl-值低于C组（P＜0.05）;T3、T4时G组K+值低于C组（P＜0.05）。与G组比较,T3、T4时F组Na+、K+值高于G组（P＜0.05）;T4时F组Cl-值高于G组（P＜0.05）。T2、T3、T4、T5时C组、F组的Glu值低于G组（P＜0.05）。结论 在婴儿的胃肠道手术中输注复方电解质液更为理想。     

Prevention of ischemic acute renal failure with impermeant solutes

Studies were performed to evaluate the effect of solute permeability and extracellular osmolality in protecting against ischemic acute renal failure. The functional protective effect of a 1-min intrarenal perfusion (prior to intrarenal norepinephrine 0.75 micrograms . kg-1 . min-1) of a hypertonic permeant solute (hypertonic saline, 1,400 mosmol/kg H2O) and an isotonic impermeant solute (isotonic mannitol, 280 mosmol/kg H2O or isotonic polyethylene glycol, IPEG, 300 mosmol/kg H2O) was evaluated. Three hours after ischemia, the glomerular filtration rate was significantly lower in hypertonic saline group vs. either the isotonic mannitol- or IPEG-treated animals (2.4 vs. 8.9 and 10.4 ml/min, respectively; both P less than 0.05). Mean renal blood flow was similar in all three groups. The effects of hypertonic saline and IPEG on glomerular filtration pressure and tubular obstruction were also evaluated. Stop-flow pressure, as an index of glomerular filtration pressure, was higher in the IPEG- vs. the hypertonic saline-treated animals (40 vs. 35 mmHg, P less than 0.001). Although proximal tubular pressure was increased in both groups, transglomerular hydrostatic pressure was higher in the IPEG vs. the hypertonic saline group (13 vs. 6 mmHg, P less than 0.01). Tubular microperfusion studies demonstrated increases in proximal tubular pressure in the hypertonic saline but not the IPEG studies. The present results indicate that isotonic, impermeant solutes provide functional protection against ischemic acute renal failure. The beneficial effect of impermeant solute is mediated, at least in part, by better maintenance of transglomerular hydrostatic pressure and prevention of secondary tubular obstruction.     

Edta chelation therapy: an ethical problem.

The randomized, double-blind study is generally regarded as the ideal standard of clinical drug trials, but uncritical blinding in clinical studies should be questioned (1,2). Most often, the method of randomization is not sufficiently described. There are examples of researchers having used opaque envelopes or opened several envelopes or X-rayed the envelopes. Violation of the randomization is unfortunately common (3). New guidelines for structured reporting of clinical trials with focus on the randomization method have been worked out (4). However, other methods of violation of the randomization have not been covered in the new guidelines. In a claimed double-blind multi-center study, isotonic Na2 ethylenediaminetetraacetic acid (edta) solution as verum and isotonic saline as placebo was used without any problem with the blinding. In the multi-center study, only nine incidents of burning at the infusion site were registered out of a total of more than 1000 Na2edta infusions (5). In our study, a total of 10 persons were given exactly the same kind of infusions and nine out of 10 receiving Na2edta infusions reacted with burning at the infusion site, thus proving it impossible to use Na2edta versus saline and maintain the blinding in a study of double-blind design. The difference in painful reactions between the Na2edta group and the saline group at the infusion site is statistically significant (P<0.001).     

Analysis of unidirectional fluxes of sodium during diarrhea induced by Clostridium perfringens enterotoxin in the rat terminal ileum.

Net intestinal transport of sodium in vivo, in control and enterotoxin (Clostridium perfringens)-treated rats, was resolved into two unidirectional fluxes, influx from and efflux into the lumen of the terminal ileum. In rats treated with the toxin, sodium influx remained similar to control values even during fluid and electrolyte loss to the lumen. Net loss of sodium was shown to be due to nearly a twofold increase in sodium efflux to the lumen in toxin-treated animals. There was only slight histopathological damage to the mucosa, especially noticeable at the tips of villi.     

Atriopeptins and renal cortical and papillary blood flow

Studies were made of the effect of two pure synthetic atrial natriuretic factors (ANF) on renal cortical and papillary blood flow and on the excretion of sodium, potassium and water in young Munich Wistar rats by means of laser-Doppler flowmetry. The effects of Atriopeptin I (AP I), which selectively relaxes intestinal smooth muscle, were compared with those of Atriopeptin II (AP II), which relaxes both vascular and intestinal smooth muscle. Both peptides were administered by continuous intravenous infusion at 10 μg h^-1 kg^-1 body wt after a control period. A time control group was studied in parallel to see whether the variables investigated varied with time. In rats receiving vehicle alone (time control) and in those receiving AP I, there was no significant change either in the cortical or papillary blood flow, or in blood pressure (BP). The AP II infusion resulted in an increase in blood flow which was only transient despite the continous infusion. Cortical blood flow increased by 22% (peak value) and papillary blood flow increased by 95% (peak value). The blood pressure (BP) decreased by 12% to a steady state level (103 ± 2 vs. 91 ± 2 mm Hg). The AP I caused a steady two-fold increase in sodium excretion (U_NaV), a 35 % increase in potassium excretion (U_KV) and an 85% unsient increase in urine flow rate (V). Infusion of AP II resulted in a more than 60-fold increase in U_NaV during the period of increased blood flow, and then reached a steady state level 10 times higher than the control value. The U_KV increased four-fold and then reached a steady state level 60% above the control value. The urine flow rate showed a 10-fold increase and then reached a steady state level 85% above the control value. In conclusion, AP I and AP II appear to increase solute excretion predominantly by affecting tubular transport mechanisms. The AP II, through its vascular effects, will transiently increase renal blood flow, preferentially in the inner medulla, and presumably the glomerular filtration rate (GFR), which in turn will contribute to the natriuretic response.,     

The effect of renal arterial infusion of albumin on renal function in the rat

Summary An infusion of an isotonic saline solution or of the same solution to which human serum albumin had been added in a concentration of 6 and 25% was administered into the renal artery of rats. The sodium and water excretion and the inulin and PAH clearances were not different when isotonic saline solution or 6% albumin were applied. After an infusion of 25% albumin solution a transient natriuresis and diuresis, accompanied by an increase of blood pressure, was observed. These experiments do not support the hypothesis which suggests the importance of peritubular oncotic pressure for the reabsorption of fluid and sodium in the rat renal tubules.     

Influence of ruminal water-loading on renal sodium excretion and water intake following feeding in sheep.

We investigated the effect of ruminal water loading before feeding on the natriuretic and drinking responses that follow feeding. Six sheep fed 800 g of chaff drank 1360 +/- 150 mL during the 5 h immediately following feeding and increased renal Na excretion. Plasma Na concentration increased by 4 mmol L (-1) and plasma osmolality by 9 mosmol kg (-1) within 1.5 h and remained elevated. A rumen load of water administered before feeding prevented the increases in plasma Na and osmolality without affecting feeding. The natriuresis, water drinking and vasopressin secretion in response to feeding were abolished. Total sodium excreted during the experiment was halved in water-loaded animals compared with untreated animals (30.4 +/- 2.1 mmol (-1) cf. 63.8 +/- 2.9 mmol-1; P < 0.01). Ruminal loading with isotonic saline caused a 33% reduction in postprandial drinking, however, reducing cerebrospinal fluid NaCl concentration abolished postprandial drinking and natriuresis. Intravenous infusion of isotonic dextran appeared to delay the onset of water intake without changing the total volume of water drunk, suggesting a role of plasma volume in initiating drinking. We conclude from the data that central osmoregulatory mechanisms that include increased sodium excretion as well as thirst and vasopressin release are activated following food intake by sheep.     

Water and sodium excretion in unilaterally denervated normal and sodium depleted anesthetized rats before and after plasma volume repletion

The possible role of a reduction in plasma volume (PV) by surgery as well as the importance of dietary Na supply in denervation natriuresis have been investigated on Inactinanesthetized male rats subjected to acute unilateral renal sympathectomy. Four groups were studied: I. Normal Na diet (n=14); II. Low Na diet (boiled rice for 2 weeks)-isotonic glucose infusion (n=10); III. Low Na diet-isotonic saline infusion (n=5); IV. Normal and low Na diet rats served as conscious control (n=10). Surgery caused a 9–11% increase in hematocrit and a 15–18% decrease in PV in groups I–III. Plasma volume repletion (PVR) reverted these changes. In group I sodium excretion from both kidneys was only a fraction of that in conscious animals kept on the same diet (group IV) and marked denervation natriuresis was observed. After PVR sodium output of innervated (I) kidneys was not different from that of conscious rats but denervated (D) kidneys excreted twice that amount. In group II Na excretion was increased compared to conscious Na depleted controls, and PVR augmented further this difference. Surprisingly, the difference in urinary sodium excretion (U_NaV) between I and D kidneys was absent after surgery and was minimal after PVR in this group. In group III physiological saline infusion reverted the effect of Na depletion and denervation natriuresis was present both before and after PVR. It is concluded that PV reduction does not play a major role in denervation phenomenon. In Na depleted anesthetized rats denervation natriuresis is absent or minimal.     

Cardiovascular effects of salbutamol in rabbits anesthetized with sodium pentobarbital

1) Heart rate, instantaneous carotid blood flow (electromagnetic probe) and arterial blood pressure were recorded for 60 minutes in rabbits anesthetized with sodium pentobarbital (40 mg/kg). Anesthetic induction was made one hour before starting the measurements to allow animal preparation. These measurements were performed on three experimental groups--(A) group: anesthetized animals without any treatment (control group); (A + SA) group: anesthetized animals + intravenous (I.V.) infusion of salbutamol (300 micrograms/kg); (A + SE) group : anesthetized animal + I.V. infusion of a saline solution in the same volume and time conditions than for (A + SA) group, that is to say (10 ml within 10 min): this series was conducted to explore the specific effects of hypervolemia. 2) Comparing the SE and SA groups, it appeared, within 30 to 120 seconds, that I.V. infusion of salbutamol induced a decrease in systolic and diastolic blood pressures and a significant increase in heart rate and carotid blood flow. While heart rate and blood pressures returned progressively to their control values (A group), carotid blood flow was still higher 60 minutes after starting salbutamol infusion. 3) The possible mechanisms involved in the observed cardiovascular responses to salbutamol are discussed. The predominant effect is probably the hypotension resulting from a peripheral vasodilatation by direct stimulation of beta 2-adrenergic receptors in vascular smooth muscle. The increase in heart rate and carotid blood flow may be explained by a two fold mechanisms: direct stimulation of the beta-adrenergic receptors (beta 1 and/or beta 2) and consequences of the vasodilatation.     

Influence of ruminal water‐loading on renal sodium excretion and water intake following feeding in sheep

We investigated the effect of ruminal water loading before feeding on the natriuretic and drinking responses that follow feeding. Six sheep fed 800 g of chaff drank 1360 ± 150 mL during the 5 h immediately following feeding and increased renal Na excretion. Plasma Na concentration increased by 4 mmol L^–1 and plasma osmolality by 9 mosmol kg^–1 within 1.5 h and remained elevated. A rumen load of water administered before feeding prevented the increases in plasma Na and osmolality without affecting feeding. The natriuresis, water drinking and vasopressin secretion in response to feeding were abolished. Total sodium excreted during the experiment was halved in water‐loaded animals compared with untreated animals (30.4 ± 2.1 mmol^–1 cf. 63.8 ± 2.9 mmol^–1; P < 0.01). Ruminal loading with isotonic saline caused a 33% reduction in postprandial drinking, however, reducing cerebrospinal fluid NaCl concentration abolished postprandial drinking and natriuresis. Intravenous infusion of isotonic dextran appeared to delay the onset of water intake without changing the total volume of water drunk, suggesting a role of plasma volume in initiating drinking. We conclude from the data that central osmoregulatory mechanisms that include increased sodium excretion as well as thirst and vasopressin release are activated following food intake by sheep.