Changes in hemodynamics with advancing age in conscious spontaneously hypertensive rats

The changes of hemodynamics were measured in spontaneously hypertensive rats (SHR) of increasing ages. Male SHR and Wistar rats of the Kyoto strain (WKY) at 4, 12, 24 and 48 weeks of age were used. The right jugular vein and the left femoral artery were cannulated and a thermistor was placed in the ascending aorta. After 24-hour rest, heart rate (HR), mean arterial pressure (MAP) and cardiac output (CO) were measured. The ratio of left ventricular weight (LVMI) of 4 week-old SHR had already increased significantly when compared to WKY. The HR in 4-week-old SHR was significantly higher than WKY. The increased HR in young SHR indicates the hypersensitivity of the sympathetic nervous system. Increased CO in 4 week-old SHR was due to high HR. The ratio of heart work to left ventricular mass (HW/LVM) of SHR at all age groups was not different from that of WKY, although the ratio of heart work to body weight (HWI) had a tendency to rise in SHR as compared to that in WKY. Our conclusion is that the development of LVM adapts to HW.     

Ramipril improves hemodynamic recovery but not microvascular response to ischemia in spontaneously hypertensive rats

BACKGROUND: Angiotensin converting enzyme (ACE) inhibition exerts positive effects on the microvasculature of normotensive animals, although this concept is not universally accepted. Recently, ACE inhibitors have been suggested to be useful for rescue in peripheral ischemia. METHODS: We investigated whether chronic treatment with the ACE inhibitor ramipril may have a positive impact on the defective healing response to ischemia that is typical of spontaneously hypertensive rats (SHR). Unilateral limb ischemia was induced in 20-week-old SHR by surgically removing the left femoral artery. Rats were allowed to regain consciousness and then were randomly allocated to treatment with ramipril (1 mg/kg body weight in drinking water) or vehicle for 28 days. RESULTS: The SHR failed to develop reparative angiogenesis in response to ischemia, thus having inadequate perfusion recovery. Ramipril reduced both tail-cuff systolic blood pressure (180 +/- 7 v 207 +/- 2 mm Hg in the vehicle group at 28 days, P < .05) and intra-arterial mean blood pressure (115 +/- 6 v 135 +/- 5 mm Hg in the vehicle group, P < .05). These effects were associated with increased responsiveness to endothelium-dependent vasodilatation by acetylcholine. Treatment with ramipril did not influence muscular capillary and arteriole density but accelerated the rate of perfusion recovery, leading to complete healing within 28 days after surgery. CONCLUSIONS: These results indicate that ACE inhibition by ramipril may be useful for the treatment of peripheral vascular complications in hypertension.     

Exaggerated response to alerting stimuli in spontaneously hypertensive rats

The startle response, consisting of behavioral and cardiovascular components, was used to study the reaction of the cardiovascular system to a mild environmental stressor. We used tactile air puff startle to study responses in adult Wistar-Kyoto and spontaneously hypertensive rats. In both strains, air puff elicits a transient motor response with rapid habituation over the test session of 30 trials. Spontaneously hypertensive rats exhibit exaggerated motor responses compared with Wistar-Kyoto rats. Similarly, a 2-3-second duration pressor response was significantly greater in spontaneously hypertensive rats than in Wistar-Kyoto rats (47.7 +/- 2.0 versus 37.1 +/- 1.5 mm Hg, respectively). However, spontaneously hypertensive rats and Wistar-Kyoto rats exhibited strikingly dissimilar heart rate responses. Wistar-Kyoto rats exhibited a transient bradycardia (-42 +/- 7 beats/min) on early trials yielding to tachycardia on later trials (35 +/- 11 beats/min). In contrast, spontaneously hypertensive rats exhibited only tachycardia to all stimuli with an absence of bradycardia. Adrenal medullary secretions chronically modulate cardiac responses in both strains. Sinoaortic denervation did not alter the magnitude or profile of the heart rate responses. Spontaneously hypertensive--Wistar-Kyoto rat differences were not secondary to hypertension because renovascular hypertensive Wistar-Kyoto rats show normal responses to air puff. Four-week-old spontaneously hypertensive rats exhibit enhanced pressor and suppressed bradycardia responses relative to age-matched Wistar-Kyoto rats, indicating chronotropic differences precede development of established hypertension. Our results indicate parasympathetic activation by the mild startle stimuli rather than sympathetic withdrawal allows bradycardia to mask a latent tachycardia in Wistar-Kyoto rats. Spontaneously hypertensive rats exhibit a parasympathetic insufficiency in the startle response to novel alerting stimuli. Thus, mild air puff startle identifies a unique and discriminatory phenotypic difference between inbred normotensive and hypertensive rats.     

Rapid hypotensive response to fasting in spontaneously hypertensive rats

This study examined changes in renal function and mean arterial pressure (MAP) in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats during 48 h of fasting, independent of changes in sodium intake. Spontaneously hypertensive rats (n = 17) and WKY rats (n = 10) were instrumented with artery and vein catheters and sodium intake was clamped at 2.1 mEq/day. By day 2 of fasting, MAP decreased −10 ± 1 mm Hg (P < .001) in SHR, but did not change significantly in WKY rats. Heart rate decreased significantly in both groups by day 2 of fasting and there was a significant increase in urine volume and sodium excretion. Thus, fasting caused a rapid decrease in MAP in SHR that was not due to decreased sodium intake, but may be related, in part, to volume loss and improved renal excretory function.     

Long-term microvascular response to hydralazine in spontaneously hypertensive rats

Chronic microcirculatory alterations produced by prolonged use of a vasoactive drug were repeatedly observed in the same skeletal muscle vessels of the dorsal microcirculatory chamber. Arterioles and venules with diameters averaging from 70 to 90 microns, the size range contributing most to peripheral vascular resistance, were measured daily for 6 days to determine differences in diameter, tortuosity, and number of branches. Hydralazine was given as a subcutaneous pellet (2.5 mg), with a release life of 21 days. Hydralazine caused a 39% dilation in arterioles of Wistar-Kyoto rats (WKY) at 3 hours but only an 8% dilation in those of spontaneously hypertensive rats (SHR). At 6 hours, arterioles in both groups were similarly dilated (30-33%). Beyond 6 hours, both SHR and WKY arterioles returned to their prehydralazine control diameter, even though arterial pressure was still reduced. By Day 6, in WKY, but not SHR, there was an increase in the tortuosity of arterioles and a tendency for an increase in their number. Venous diameter was also increased on Day 6, consistent with the fluid retention effect of hydralazine. These data indicate that some so-called vasodilators may cause long-term alterations in growth of vessels rather than an increase in vessel caliber.     

Cardiovascular responses to acute stress in young-to-old spontaneously hypertensive rats

Age-related changes in circulatory responses to short-term shaker stress were investigated in conscious spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Hemodynamics (microspheres) were measured at 8, 24, 48, and 96 weeks of age, and plasma catecholamines were measured at 8 and 96 weeks. At rest, elevated mean arterial pressure was associated with unaltered cardiac index and heart rate in SHR compared with WKY at all ages. Regional blood flow was largely similar in both strains, except for a reduced renal flow in 96-week-old SHR. Cardiac index and most regional blood flow tended to or did decline in both strains between 8 and 96 weeks. Plasma catecholamines were similar in both strains at 8 and 96 weeks. Shaker stress evoked responses similar to defense reactions in both strains. The incremental responses in mean arterial pressure, heart rate, cardiac index, and cerebral, skeletal muscle, and myocardial flow and the decremental responses in splanchnic, renal, and skin flow were greater in SHR than in WKY, particularly at 8 weeks. Most of these responses tended to or did decline between 8 and 96 weeks in both strains. The plasma catecholamine responses were also greater in SHR at 8 and 96 weeks, and they did not differ in either strain between these ages. Thus, circulatory and sympathoadrenal reactivity to acute stress were enhanced in SHR compared with WKY, independently of age.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in growth hormone secretion in spontaneously hypertensive rats

Secretion of the growth hormone (GH) in spontaneously hypertensive (SH) male rats has been determined and compared with that of normotensive Wistar-Kyoto (WKY) controls. In a first set of experiments, plasma GH concentration and pituitary GH content were measured in SH rats 30, 60 and 90 days old. 30-day rats showed reduced GH plasma and pituitary levels, whereas in 60- and 90-day-old rat no differences in GH plasma concentration and increased GH pituitary content were observed. In a second set of experiments, 90-day-old SH male rats anesthetized with sodium pentobarbital and intravenously injected with growth hormone-releasing factor (GRF) showed an amplitude and duration of response to injected hormone higher than WKY controls. In a third set of experiments, hemipituitaries of 90-day-old SH males were incubated for 2 h in Krebs-Ringer-bicarbonate either in the presence or in the absence of GRF. In the absence of GRF stimulation, the in vitro release of GH was higher than in WKY controls, whereas in the presence of GRF the sensitivity and the maximum response to GRF was reduced in comparison with normotensive male rats. These results indicate that SH rats have decreased pituitary content and plasma GH concentration before puberty. Besides, they showed increased pituitary GH content in adulthood and opposite changes in the in vivo and in vitro response to GRF.     

Exaggerated depressor response to 6-iodoamiloride in NaCl-sensitive spontaneously hypertensive rats

The current study tested the hypothesis that NaCl-sensitive hypertension may result from increased membrane sodium channel activity. The effect of 6-iodoamiloride, and analog of the sodium channel blocker amiloride, on mean arterial pressure (MAP) was examined in conscious, freely moving NaCl-sensitive spontaneously hypertensive rats (SHR-S) fed high (8%) or normal (1%) NaCl diets. SHR-S and age-matched NaCl-resistant SHR (SHR-R) and normotensive Wistar-Kyoto (WKY) control rats were studied at 9 weeks of age after 2 weeks on either high (8%) NaCl or control (1%) NaCl diets. 6-iodoamiloride was infused intravenously in doses of 0.38 or 0.76 mg/100 g body weight, and MAP and heart rate (HR) were monitored from a femoral arterial cannula for 2 hours. The 8% NaCl diet caused a significant elevation in MAP in SHR-S but not in SHR-R or WKY. Administration of 6-iodoamiloride (both doses) produced a significant, sustained decrease in MAP in both SHR-S and SHR-R. Maximal depressor responses to high dose 6-iodoamiloride were significantly enhanced in SHR-S fed 8% NaCl (31.2 +/- 3.7 mm Hg) compared to SHR-S fed 1% NaCl (14.8 +/- 2.4 mm Hg) or SHR-R fed either 8% or 1% NaCl diets (15.6 +/- 4.2 and 10.2 +/- 3.0 mm Hg, respectively). In contrast, feeding an 8% NaCl diet had no significant effect on the depressor responses to 6-iodoamiloride in either SHR-R or WKY rats. In WKY, these doses of 6-iodoamiloride had no significant effect on MAP in either diet group. 6-iodoamiloride had no significant effect on heart rate in any group. These results support the hypothesis that the exacerbation of hypertension in SHR-S fed a high NaCl diet may result from increased membrane sodium channel activity.     

Impaired reflex response to volume expansion in NaCl-sensitive spontaneously hypertensive rats

Abnormal baroreceptor reflex function that antedates or is a consequence of NaCl loading could contribute to the NaCl-induced exacerbation of hypertension in NaCl-sensitive spontaneously hypertensive rats (SHR-S). The current study tested the hypothesis that an impairment in cardiopulmonary baroreceptor reflex function exists in SHR-S before NaCl loading. The reflex response to volume expansion was compared in SHR-S, NaCl-resistant SHR (SHR-R), and normotensive Wistar-Kyoto (WKY) and Sprague-Dawley rats maintained on a normal NaCl diet. Conscious, free-moving SHR-S, SHR-R, WKY, and Sprague-Dawley rats were volume expanded with whole blood to 15% of blood volume within 6 minutes, and mean arterial pressure, heart rate, and lumbar sympathetic nerve activity were recorded. Heart rate and lumbar sympathetic nerve activity decreased significantly in SHR-R, WKY, and Sprague-Dawley rats after volume expansion. In contrast, in SHR-S neither heart rate after volume expansion nor lumbar sympathetic nerve activity was significantly different from levels before volume expansion. The blunted reflex response of heart rate and lumbar sympathetic nerve activity to volume expansion suggests impaired cardiopulmonary volume receptor function in SHR-S. This likely contributes to NaCl-induced hypertension in SHR-S on a high NaCl diet.     

Enhanced sympathetic-adrenal medullary response to cold exposure in spontaneously hypertensive rats

To investigate the regulation of sympathetic-adrenal medullary function in spontaneously hypertensive (SHR) male rats, we measured urinary catecholamine excretion for 4 h at room temperature and also during cold exposure (4 degrees C) in groups of four and 12-week-old stroke-prone SHR (SHRSP), stroke-resistant SHR (SHRSR) and normotensive Wistar-Kyoto (WKY) rats. The effect of cold exposure on 12-week-old adrenal denervated rats was also examined. At room temperature, urinary excretion of epinephrine, but not norepinephrine or dopamine, was increased significantly in four-week-old SHRSP and SHRSR rats compared with age-matched WKY. The enhanced excretion of epinephrine at room temperature was not observed in hypertensive rats at 12 weeks of age. During cold exposure, urinary concentrations of each catecholamine increased markedly in rats of all three strains. In addition, the epinephrine response was significantly enhanced in SHRSP rats and the norepinephrine, epinephrine and dopamine responses were significantly enhanced in SHRSR rats. Following adrenal denervation, the urinary epinephrine response to cold exposure was abolished in all strains. These results reveal an enhancement of sympathetic and neurally-mediated adrenal medullary responses in prehypertensive SHR rats and a greater urinary epinephrine response to cold exposure in four and 12-week-old SHR rats. This alteration in catecholamine secretion may be important in the development and maintenance of this type of experimental hypertension.     

Contribution of fluid shear response in leukocytes to hemodynamic resistance in the spontaneously hypertensive rat

The mechanisms for elevation of peripheral vascular resistance in spontaneously hypertensive rats (SHR), a glucocorticoid-dependent form of hypertension, are unresolved. An increase in hemodynamic resistance caused by circulating blood may be a factor. Physiological fluid shear stress induces a variety of responses in circulating leukocytes, including pseudopod retraction. Due to high rigidity, leukocytes with pseudopods have greater difficulty to pass through capillaries. Because SHR have more circulating leukocytes with pseudopods, we hypothesize that inhibition of the leukocyte shear response by glucocorticoids in SHR impairs normal leukocyte passage through capillaries and causes enhanced resistance in capillary channels. Fluid shear leads to retraction of pseudopods in normal leukocytes, whereas shear induces pseudopod projection in SHR and dexamethasone-treated Wistar rats. The high incidence of circulating leukocytes with pseudopods results in slower cell passage through capillaries under normal blood flow and during reduced flow enhanced capillary plugging both in vivo and in vitro. SHR blood requires higher pressure (90.0+/-8.2 mm Hg) than Wistar Kyoto rat (WKY, 69.6+/-6.5 mm Hg; P<0.0001) or adrenalectomized SHR (73.5+/-2.1 mm Hg; P=0.0009) at the same flow rate in the resting hemodynamically isolated skeletal muscle microcirculation. Intravenous injection of blood from SHR, but not WKY, causes blood pressure increase in normal rats, which depends on pseudopod formation. We conclude that in addition to enhanced vascular tone, pseudopod formation with lack of normal fluid shear response may serve as mechanisms for an elevated hemodynamic resistance in SHR.     

Acute hemodynamic effects of ethanol in conscious spontaneously hypertensive and normotensive rats

This study investigated the differential hemodynamic effects of small to high doses of ethanol in conscious age-matched spontaneously hypertensive rats (SHRs) and Wistar Kyoto rats (WKYs). Changes evoked by ethanol (0.25, 0.5, or 1 g/kg, i.v.) or equal volume of saline in mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), stroke volume (SV), and total peripheral resistance (TPR) were followed for 90 min in the two rat strains. The baseline MAP (163 +/- 4 vs. 113 +/- 2 mm Hg) of SHRs was significantly (p < 0.05) higher, compared with WKYs due mainly to the presence of an elevated TPR 13.82 +/- 0.12 vs. 2.51 +/- 0.09 mm Hg/ml/min/100 g, p < 0.05) in SHRs. In both rat strains, all doses of ethanol produced immediate increases in MAP at 1 min, after which the MAP responses varied and depended on the rat strain and dose of ethanol used. In WKYs, 0.25 g/kg ethanol had no effect on MAP, but caused significant decreases in CO and SV and increased HR. Ethanol (0.5 and 1 g/kg) produced a short-lived (10 min) and dose-related increase in MAP. The higher dose (1 g/kg) of ethanol elicited significant (p < 0.05) increases in TPR that were counterbalanced by concomitant decreases in CO and SV. In SHRs, the two higher doses (0.5 and 1 g/kg) of ethanol elicited significant (p < 0.05) decreases and increases in MAP, respectively, compared with control (saline-treated) values. The pressor response to the 1 g/kg dose of ethanol was associated with an increase in TPR that achieved a statistical significance (p < 0.05) at 50 and 80 min after ethanol administration. HR was significantly (p < 0.05) reduced by the two higher doses of ethanol, whereas SV and CO were not changed. Blood ethanol concentrations measured 10, 30, and 60 min after ethanol administration were similar in SHRs and WKYs. These findings suggest that acute administration of ethanol to conscious rats elicits hemodynamic responses that are strain- and dose-dependent. In contrast to a short-lived and dose-related pressor response in WKYs, ethanol (0.5 and 1 g/kg) elicited opposite and longer lasting effects on MAP (decreases and increases, respectively) in SHRs. In both rat strains, the pressor response to the higher dose of ethanol was associated with an increase in TPR; an effect that was compromised by a concomitant decrease in CO in WKYs but not SHRs.     

Clonidine abolishes exaggerated pressor responses to shaker stress in spontaneously hypertensive rats

To determine whether clonidine would attenuate exaggerated pressor responses to stress in spontaneously hypertensive rats (SHR), pressor responses to shaker stress were recorded following intracerebroventricular (icv) injections of clonidine in conscious SHR. Pressor responses to shaker stress were significantly larger in SHR than in Wistar-Kyoto rats (WKY). Increased sympathetic nerve responses to shaker stress were also significantly greater in SHR than in WKY. Exaggerated pressor responses in SHR were partly attenuated by adrenalectomy and abolished by clonidine (icv). By contrast, 1-Sar,8-Ile angiotensin II (icv) was ineffective. These findings suggest that in SHR, the alpha-adrenergic system in the brain may contribute to exaggerated pressor responses to shaker stress, but not the brain renin-angiotensin system.     

Changes in follicle-stimulating hormone secretion in spontaneously hypertensive rats.

FSH and testosterone plasma levels, pituitary FSH content and concentration and the weight of testis, seminal vesicles and ventral prostate have been studied at the ages of 30, 60 and 90 days in spontaneously hypertensive rats (SHR) and normotensive control (WKY) rats. In vitro FSH secretion by pituitaries, and the response to orchidectomy and to exogenous administration of either LHRH (1 microgram) or LHRH agonist (0.05, 0.1, 1, and 5 micrograms/kg) were analyzed in 90-day-old SHR and WKY male rats. Ventral prostate weight and FSH plasma levels were determined in other groups of adult male rats castrated and castrated and implanted for 15 days with silastic capsules containing testosterone, dihydrotestosterone or estradiol. Also FSH plasma levels and pituitary FSH concentration were determined at the ages of 30, 60 and 90 days in SHR and WKY female rats. Male SHR showed increased plasma FSH levels and high testicular weight in all the cases, and enhanced testosterone levels in plasma and pituitary FSH content on days 60 and 90. Weight of seminal vesicles and ventral prostate was normal or reduced, depending on the animal age. Adult SHR had increased FSH secretion in vitro, normal response to orchidectomy and did not exhibit FSH increases after LHRH administration. The efficiency of testosterone to stimulate ventral prostate growth and the ability of estradiol to reduce FSH plasma levels were decreased in SHR. Female SHR showed a significant increase in the pituitary content of FSH on day 30 and on proestrus at the ages of days 60 and 90.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of age on contractile response to insulin-like growth factor 1 in ventricular myocytes from spontaneously hypertensive rats

Evidence suggests a pathophysiological role of insulin-like growth factor 1 (IGF-1) in hypertension. Cardiac function is altered with advanced age, similar to hypertension. Accordingly, the effects of IGF-1 on cardiac myocyte shortening and intracellular Ca(2+) were evaluated in hypertension at different ages. Ventricular myocytes were isolated from Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), aged 12 and 36 weeks. Mechanical and intracellular Ca(2+) properties were examined by edge-detection and fluorescence microscopy. At 12 weeks, IGF-1 (1 to 500 ng/mL) increased peak twitch amplitude (PTA) and FFI changes (DeltaFFI) in a dose-dependent manner in WKY myocytes, with maximal increases of 27.5% and 35.2%, respectively. However, IGF-1 failed to exert any action on PTA and DeltaFFI in the age-matched SHR myocytes. Interestingly, at 36 weeks, IGF-1 failed to exert any response in WKY myocytes but depressed both PTA and DeltaFFI in a dose-dependent manner in SHR myocytes, with maximal inhibitions of 40.5% and 16.1%, respectively. Myocytes from SHR or 36-week WKY were less sensitive to norepinephrine (1 micromol/L) and KCl (30 mmol/L). Pretreatment with nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME, 100 micromol/L) did not alter the IGF-1-induced response in 12-week WKY myocytes but unmasked a positive action in 12-week SHR and 36-week WKY myocytes. L-NAME also significantly attenuated IGF-1-induced depression in 36-week SHR myocytes. In addition, the Ca(2+) channel opener Bay K8644 (1 micromol/L) abolished IGF-1-induced cardiac depression in 36-week SHR myocytes. Collectively, these results suggest that the IGF-1-induced cardiac contractile response was reduced with advanced age as well as with hypertension. Alterations in nitric oxide and intracellular Ca(2+) modulation may underlie, in part, the resistance to IGF-1 in hypertension and advanced age.     

Some enzyme characteristics of spontaneously hypertensive rats myocardium

In order to ascertain the pathogenesis of myocardial cell vulnerability in spontaneously hypertensive rats (SHR), several enzyme activities were examined by using subcellular fractions of myocardium and compared to those in Wistar-Kyoto rats (WKY). In the normotensive WKY heart, both 5'-nucleotidase and Na+/K(+)-ATPase, which are plasma membrane associated enzymes, increased with age. But in the SHR heart, both enzymes were lower at 16 weeks than they were at 10 weeks of age. Moreover, at 16 weeks of age they were lower in SHR than in WKY. On the other hand, NADP(+)-isocitrate dehydrogenase activity, a mitochondria associated enzyme, was higher in SHR than in WKY at 6 weeks, but lower at 10 and again at 16 weeks of age. The activities of both acid phosphatase and N-acetyl-beta-glucosaminidase, which are lysosomal enzymes, decreased with age in SHR but not in WKY. These results suggest that an enzymatic alteration in the plasma membrane and mitochondria may be one of important factors behind myocardial vulnerability in the SHR heart.     

Changes in cardiac beta-adrenoceptor concentrations in spontaneously hypertensive and experimental renal hypertensive rats

Cardiac beta-adrenoceptors were studied in membrane fractions from spontaneously hypertensive rats (SHR) and rats with two-kidney, one clip hypertension (2K, 1C HT), using radioligand binding method. beta-Adrenoceptor concentration measured by [3H]-dihydroalprenolol (DHA) binding was significantly lower in cardiac membranes from two months old SHR than those from Wistar-Kyoto rats (WKY) (38.2 +/- 2.6 vs 45.1 +/- 1.8 fmol/mg protein, means +/- SEM, p less than 0.05). Cardiac membranes from 2K, 1C HT rats had also a lower concentration of beta-adrenoceptors than those from the sham-operated control rats at a week after operation (30.9 +/- 2.2 vs 47.8 +/- 1.6 fmol/mg protein, p less than 0.01). But receptor affinity remained unchanged. These reduced concentrations of beta-adrenoceptors were restored to control levels at 12 months old in SHR and at 6 weeks after operation in 2K, 1C HT rats, although age-dependent decrease in beta-adrenoceptor was observed. The decrease in beta-adrenoceptor was associated with increase in plasma noradrenaline levels during the earlier stages of hypertension. But there is no correlation between beta-adrenoceptor concentrations and plasma noradrenaline levels in the chronic stages of hypertension. No significant difference was found in activities of 5'-nucleotidase, which is a marker enzyme of cell membrane, in membrane fractions between the hypertensive hearts and the controls, suggesting that the cardiac hypertrophy is not a determinant factor for change in beta-adrenoceptor. The observed decrease in beta-adrenoceptor concentration may reflect an increase in sympathetic nerve activity during development of hypertension. In the chronic stages of hypertension, additional factors may be involved in the restoration of beta-adrenoceptors.     

Sino-aortic denervation alters the hemodynamic response to exercise in hypertensive rats.

The effect of sino-aortic denervation (SAD) on the heart rate (HR), arterial pressure (AP) and regional blood flow responses during dynamic exercise was examined in spontaneously hypertensive rats (SHR). Intact (n= 14) and SAD (n= 17) rats were instrumented with arterial catheters and mesenteric and iliac Doppler ultrasonic flow probes. After recovery, all rats underwent a graded exercise test. Heart rate increased significantly during exercise in intact and SAD rats. There was no significant difference in the steady state heart rate response to exercise in the intact and SAD rats. Arterial pressure increased during exercise in the intact rats. In sharp contrast, arterial pressure decreased during exercise in the SAD rats. Iliac vascular conductance increased during exercise in the intact and SAD rats. The increase in iliac vascular conductance during exercise was significantly greater in the SAD rats. Mesenteric vascular conductance decreased during exercise in the intact and SAD rats. The decrease in mesenteric vascular conductance during exercise was significantly attenuated in the SAD rats. Results suggest that functioning arterial baroreceptors are required for the typical hemodynamic responses during dynamic treadmill running in hypertensive rats.