Production of Arneil-Dekanski factor in vitro by plasma of renal hypertensive rats

Production of the Arneil-Dekanski factor by rat plasma in vitro was studied in different forms of experimental renal hypertension. The results suggest that this pressor activity of plasma plays no role in experimental renal hypertension

Noradrenaline: Central inhibitory control of blood pressure and heart rate

Noradrenaline injected bilaterally into the brainstem in the area of the nucleus tractus solitarii decreased systemic arterial blood pressure and heart rate of anesthetized rats. The effect of noradrenaline was prevented by a preceding injection of the α-adrenergic blocking agent phentolamine, at the same site. The results suggest an inhibitory role of an α-adrenoceptor in the area of the nucleus tractus solitarii in the central control of blood pressure

ROLE DES RECEPTEURS MINERALOCORTICOIDES DU SYSTEME NERVEUX CENTRAL DANS LA REGULATION DES FONCTIONS CARDIOVASCULAIRES ET RENALES (DOCTORAT (PHARMACOLOGIE))

STRASBOURG ILLKIRCH-Pharmacie (672182101) / SudocSudocFranceF

Endorphins and the hypotensive response to stimulation of alpha-receptors in the brainstem by alpha-methylnoradrenaline

Opioid peptide involvement in the fall in blood pressure resulting from stimulation of alpha-receptors in the brainstem has been investigated in the urethane-anaesthetised rat. Unilateral microinjection of alpha-methylnoradrenaline into the nucleus tractus solitarii (NTS) induced a doserelated fall in blood pressure and heart rate. The depressor response induced by the amine was prevented by pretreatment with naloxone, administered either subcutaneously or directly into the nucleus. Pretreatment with antiserum to beta-endorphin, applied locally, also blocked the depressor response, however a similar dilution of antiserum to met-enkephalin was ineffective in this respect. The local application of phentolamine into the n. tractus solitarii caused an initial fall in both blood pressure and heart rate, and blocked the cardiovascular changes induced by alpha-methylnoradrenaline for at least 90 min. Pretreatment with the alpha-receptor antagonist attenuated the fall in blood pressure produced by microinjection of beta-endorphin. These results suggest that the fall in blood pressure observed after administration of alpha-methylnoradrenaline involves a beta-endorphin-like peptide, a probable site of this interaction being the n. tractus solitarii

Hypotensive response in spontaneously hypertensive rats following microinjection of α-methylnoradrenaline in the caudal brain-stem

Local microinjection of 1.25 nmol (-)-α-methylnoradrenaline in the A2-region of the nucleus tractus solitarii (NTS) caused a decrease of blood pressure and heart rate in both spontaneous hypertensive rats (SHR) and Wistar-Kyoto (W/K) rats. Although the maximal responses in both strains did not differ, the decrease in blood pressure lasted longer in the SHR. These results do not support the concept of a diminished sensitivity of catecholaminergic receptors in the NTS of SHR to α-methylnoradrenaline

Augmentation of the pressor response to octapressin by autonomic blocking agents in the pithed rat

The effect of octapressin on blood pressure was studied in anesthetized pithed male rats, pretreated with autonomic blocking agents. Phenoxybenzamine and chlorpromazine induced an augmentation of the blood pressure response to octapressin, whereas atropine, propranolol and hexamethonium had no effect on the response to octapresin in the pithed rat. It is concluded that phenoxybenzamine and chlorpromazine augment the blood pressure response to octapressin in the pithed rat by a direct effect on the peripheral vascular effector cells

α-Methylnoradrenaline induced hypotension and bradycardia after administration into the area of the nucleus tractus solitarii

Bilateral injections of α-methylnoradrenaline into the area of the nucleus tractus solitarii of the brain stem caused a dose-dependent decrease of systemic arterial blood pressure and heart rate of anesthetized rats. The effects were prevented and even reversed by a preceding injection of the α-adrenoceptor blocking agent phentolamine. Pressor doses of angiotensin II and of arginine-vasopressin at the same site failed to decrease blood pressure and heart rate

Effect of autonomic blocking agents on the cardiovascular effects of octapressin in the rat

Cardiovascular effects of Octapressin were studied in anesthetized male albino rats. The effect of pretreatment with the following blocking agents was evaluated: atropine, phenoxybenzamine, propranolol, hexamethonium and chlorpromazine. A decrease in blood pressure and in heart rate was induced by phenoxybenzamine; propranolol treatment caused a decrease in heart rate and an increase in circulation time. Injections of 2, 6 and 18 mU Octapressin caused no changes in cardiac output or in central venous pressure. The increase in blood pressure following Octapressin was found to be dose-dependent in the saline-treated controls as well as in the rats pretreated with the autonomic blocking agents. The pressor response to Octapressin was increased by atropine, phenoxybenzamine, propranolol and chlorpromazine. From these data it is concluded that the increase in blood pressure following Octapressin is caused by an increase in vascular resistance in the systemic circulation

Arginine8-vasopressin inhibits centrally induced pressor responses by involving hippocampal mechanisms

Administration of arginine8-vasopressin (AVP) or prolyl-leucyl-glycinamide (PLG) into a lateral cerebral ventricle reduced the magnitude of systolic blood pressure increase (pressor response) induced by electrical stimulation of the mesencephalic reticular formation (MRF) in urethane-anesthetized rats. Bilateral destruction of the dorsal hippocampus prevented the action of AVP on the pressor response. However, the effect of PLG was only slightly reduced by hippocampal lesion. Microinjection of AVP in the dentate area of the dorsal hippocampus mimicked the action of intracerebroventricularly administered peptides. The effect of a single injection of AVP lasted at least for 60 min. Neither hippocampal damage nor peptide administrations resulted in changes in mean arterial blood pressure (basal BP). Bradycardiac response accompanied the BP increase during MRF stimulation. Hippocampal damage on intracerebroventricular administration of AVP and PLG failed to affect the cardiac response. Injection of AVP into the hippocampus tended to reduce the magnitude of cardiac responses caused by MRF stimulation. It is suggested that the inhibition by AVP of a pressor response produced by MRF stimulation involves the dorsal hippocampus. The action of PLG or related peptides seems to be, at least in part, through mechanisms not involving the hippocampus

Effect of autonomic blocking agents on the cardiovascular effects of octapressin in the rat

Cardiovascular effects of Octapressin were studied in anesthetized male albino rats. The effect of pretreatment with the following blocking agents was evaluated: atropine, phenoxybenzamine, propranolol, hexamethonium and chlorpromazine. A decrease in blood pressure and in heart rate was induced by phenoxybenzamine; propranolol treatment caused a decrease in heart rate and an increase in circulation time. Injections of 2, 6 and 18 mU Octapressin caused no changes in cardiac output or in central venous pressure. The increase in blood pressure following Octapressin was found to be dose-dependent in the saline-treated controls as well as in the rats pretreated with the autonomic blocking agents. The pressor response to Octapressin was increased by atropine, phenoxybenzamine, propranolol and chlorpromazine. From these data it is concluded that the increase in blood pressure following Octapressin is caused by an increase in vascular resistance in the systemic circulation