Nicotine-induced increases of noradrenaline turnover in discrete noradrenaline nerve terminal systems of the hypothalamus and the median eminence of the rat and their relationship to changes in the secretion of adenohypophyseal hormones

The effects of acute single doses (0.3 and 1 mg/kg) of nicotine on various hypothalamic catecholamine nerve terminal systems and on the secretion of adenohypophyseal hormones in the rat were studied. Nicotine, in a dose of 1.0 mg/kg, increased noradrenaline turnover in the median eminence and in the peri- and paraventricular hypothalamic regions. The dopamine and noradrenaline nerve terminal systems in the median eminence and the dorsomedial hypothalamic nucleus respectively were unaffected. Serum GH levels were decreased and serum prolactin levels increased after a dose of 1 mg/kg. In the presence of tyrosine hydroxylase inhibition, nicotine in a dose of 1 mg/kg, instead increased GH and also LH secretion. It is suggested that the preferential increases of noradrenaline turnover in various hypothalamic noradrenaline nerve terminal systems by nicotine may be partly responsible for the nicotine induced increases of serum prolactin, GH and LH levels observed.     

Differences in contractile activation between human myometrium and intramyometrial arteries

Small intramyometrial arteries and pieces of adjacent myometrial tissue were obtained from 25 non-pregnant women undergoing hysterectomy. Vascular and myometrial preparations were dissected, mounted in organ baths and isometric tension was recorded. Myometrial strips, but no vascular preparation, developed spontaneous contractile activity. Noradrenaline (NA) and vasopressin (VP) contracted both vessels and myometrium. Prostaglandin F_2α (PGF_2α) contracted the myometrial tissue, but had only a minor effect on the vessels. Removal of extracellular calcium almost abolished the myometrial responses to high K⁺ (124 mm)-solution, PGF_2α, NA and VP. The vascular responses remaining after this treatment were 18% (K⁺), 34% (NA) and 25% (VP) of control contractions induced by high K⁺ (124 mm). Nifedipine potently depressed myometrial contractions induced by NA and VP, but was less active against the vascular responses to these agents. In preparations exposed to calcium-free medium, nifedipine (10^-7 m) almost abolished myometrial contractions induced by calcium in the presence of K⁺ (124 mm), NA or VP. It also effectively depressed vascular responses to calcium in the presence of K⁺, but was less active if NA and VP were present. It is suggested that PGF_2α has almost no contractant effect on intramyometrial arteries, and that the activation process in these vessels is much less dependent on extracellular calcium than that of the myometrium.     

Long-lasting cardiovascular depressor response to somatic stimulation in spontaneously hypertensive rats.

It has been known that a short-lasting stimulation of the somatic afferent nerves elicits either a depressor or a pressor response depending on the stimulus parameters (Johansson 1962). In the present study cardiovascular responses were observed during and after a long-lasting sciatic nerve stimulation in conscious spontaneously hypertensive rats (SHR) and their normotensive controls, the Wistar Kyoto rats (WKR).     

Systemic and centrally mediated angiotensin II effects in the horse

The primary aim of the study was to evaluate the potential value of intravenous (i. v.) infusion of angiotensin II (AII) for phonocardiographic differential diagnosis of equine valvular insufficiency. Ten-minute AII infusions at 4.5–33 pmol kg^-1 min^-1 induced clear-cut dose-dependent rises in systemic arterial blood pressure (aBP), whereas the pulmonary aBP remained largely unaffected. It implies that i. v.infusion of All at about 10 pmol kg^-1 min^-1 could be a valuable tool for the acoustic differentiation between mitral and tricuspid valvular dysfunction in the horse. The infusion at, and above 9 pmol kg^-1 min^-1 caused increased heart rate. This chronotrophic effect was not strictly dose-dependent and exhibited significant tachyphylaxis. Angiotensin II administration at, or above 9 pmol kg^-1 min^-1 was needed to induce an urge to drink, suggesting that angiotensin-induced thirst does not appear in the euhydrated horse until the octapeptide reaches supraphysiological blood concentration. Determinations of plasma aldosterone concentration (PA) revealed comparatively high morning control values (269 ± 46 pmol^-1).Three consecutive AII infusions with 10-min intervals and at increasing dosages caused a cumulative, almost fourfold elevation of PA.The PA pattern indicated that AII-induced hypersecretion of aldosterone continued for several minutes after the end of the infusions, but also showed that the metabolic clearance of the hormone took precedency of the secretion within 20 min post-infusion. In two of the horses a fall in PA occurred during a fourth, final infusion, indicating that in these instances the previous AII administration had impoverished the store of aldosterone available for release from the adrenal cortex.     

Influence of extracellular calcium and nifedipine on α1-and α2-adrenoceptor-mediated contractile responses in isolated rat and cat cerebral and mesenteric arteries

The influence of extracellular Ca²⁺ and nifedipine on contractile responses to 10 μM noradrenaline (NA) was investigated in isolated rat and cat middle cerebral (RCA, CCA) and mesenteric (RMA, CMA) arteries. In the CCA (containing predominantly α₂-adrenoceptors), the NA-induced contractions developed considerably more slowly than in the RCA, RMA (containing mainly α₁-adrenoceptors) and CMA (sensitive to both at,- and α₂-adrenoceptor selective antagonists). The tonic component of the NA-induced contraction in the four types of artery was substantially suppressed after only short periods in Ca²⁺-free solution. In each type of artery, excluding the CCA, the contractile response to 124 mM K⁺ was more sensitive to Ca²⁺ deprivation than that to NA. This suggests that NA, besides mobilizing extracellular Ca²⁺, can also release Ca²⁺ from an intracellular pool in the RCA, RMA and CMA, but not in the CCA. Thus, α₁-adrenoceptor-mediated contractions in the RCA and RMA seem to depend on both Ca²⁺ influx and intracellular Ca²⁺ release, whereas α₂-adrenoceptor-mediated contractile responses in the CCA appear to rely almost entirely on Ca²⁺ influx. Both the maximum response and the tonic component of the NA-induced contraction were significantly more sensitive to nifedipine in the CCA than in the RCA. In comparison with the NA-induced contractions in these arteries, those in the RMA and CMA were relatively resistant to nifedipine. In the CCA exposed to NA in Ca²⁺-free medium, nifedipine almost abolished the contraction induced by re-addition of Ca²⁺, whereas in the other types of artery, Ca²⁺ re-application evoked a significant contraction also in the presence of the drug. The differential effects of nifedipine presumably reflect differences between the arteries, not only in the relative contribution of Ca²⁺ influx and intracellular Ca²⁺ release to the contractile activation, but also in the nifedipine sensitivity of the Ca²⁺ entry pathways utilized by NA. It is concluded that the mechanisms through which NA induces contraction seem to be related both to the subtype of α-adrenoceptor stimulated by NA and to the type of vessel studied.     

Effects of hay-feeding on acid/base balance,renal sodium excretion,aldosterone and vasopressin secretion in the goat

Effects of 30 min intense hay-feeding on acid/base and sodium homeostasis were studied in semi-starved goats during hyper- and euhydration. Parallel analyses of carotid and jugular blood samples revealed that feeding induced metabolic acidosis, which to some extent was subjected to respiratory compensation. The acidosis was accompanied by renal sodium retention and urinary acidification persisting for 2–3 h. The sodium retention was succeeded by an increase in renal Na excretion above the initial level. This natriuresis was most accentuated during hyperhydration. Blood samples taken for hormone assays during euhydration revealed a 15% increase in haematocrit and a significant rise in plasma aldosterone at termination of feeding. Inhibition of the water diuresis in hyperhydrated animals, and moderate increases in renal arginine vasopressin (AVP) excretion and plasma AVP were inconsistent effects of feeding. It is concluded, that simply jugular vein blood provides reliable information on the acid/base status of goats, but that the feeding schedule has to be considered in all experiments where small ruminants are used to investigate the integrated control of acid/base and sodium homeostasis.     

Effects of subacute treatment with toluene on cerebrocortical α- and β-adrenergic receptors in the rat. Evidence for an increased number and a reduced affinity of β-adrenergic receptors

Subacute treatment with toluene (80–1500 p.p.m.) produces a dose-dependent reduction of affinity and increase in density of the β-adrenergic antagonist [³H]dihydroalprenolol binding sites in the frontoparietal cortex of the male rat, while the binding characteristics of a,-adrenergic ([³H]WB 4101) and α₂^-adrenergic ([³H]p-aminoclonidine) binding sites in the same region is unaffected by this treatment as evaluated in vitro. Therefore, it is suggested that the cortical β-adrenergic receptors are particularly vulnerable to the action of toluene in vivo. It is speculated that as a result cortical β-adrenergic neurotransmission may be altered following exposure to low concentrations of toluene, possibly related to the physico-chemical properties of toluene, leading to changes in membrane fluidity.     

Assessment of sensory block in epidural anaesthesia by electric stimulation

The onset of sensory block in lumbar epidural anesthesia was investigated in 26 patients, aged 18 to 84 years, employing the loss of discrimination to cold and pinprick, as well as by determining threshold electric stimulation (threshold intensities). A standard dose of 2% mepivacaine with adrenaline, 5 μg ml^-1, (0.1 ml per cm body height) was given and the patients' ability to discriminate stimuli within dermatomes T8, T10, T12, L2, L4 and SI was investigated at five min intervals for 30 min after injection. From the results of the study it is concluded that i) The interval to peak analgesic efficacy of the anaesthetic solution used is < 30 min when assessments are based on the patients' ability to discriminate cold or pinprick but > 30 min when determinations of threshold intensities are employed, ii) Cold discrimination is lost earlier than discrimination to pinprick and at lower threshold intensities, iii) Threshold intensities describe the time course of onset of sensory block more precisely than results of testing by cold or pinprick, iv) The onset of sensory block was found to be positively correlated to the age of patients in the following respects: a) Threshold intensities during early onset in all investigated dermatomes except L2. b) Intensity of block in T8, T10, and SI at the end of the study period, c) Time to loss of discrimination to cold and pinprick in T12, L2 and SI, and d) Threshold intensities at loss of discrimination to cold and pinprick. We propose that determinations of threshold intensities offer distinct advantages over conventional testing by cold and pinprick discrimination, especially when detailed analyses of the sensory blocking effects of local anaesthetic drugs are being investigated.