Virtually every blood vessel in the body is surrounded to some degree by adipose tissue. A potential role for perivascular adipose tissue as a neurohumoral regulator of vascular responsiveness was studied. Thoracic aortae obtained from male Sprague-Dawley rats were cut into rings for use in a standard in vitro smooth muscle bath set-up. The vessels were either cleaned of surrounding adipose tissue or left intact. Contractile responses to KCl and phenylephrine as well as relaxation responses to acetylcholine, isoproterenol and sodium nitroprusside were not different between cleaned and intact tissues. However, a significant decrease in the sensitivity to norepinephrine was observed in intact vessels. This altered response was corrected by prior treatment with desipramine plus deoxycorticosterone. Contractile responses of aortic ring preparations to tyramine and a potassium-free physiological solution were significantly greater in intact tissues. Electrical stimulation resulted in no response in cleaned tis...

Influence of Perivascular Adipose Tissue on Rat Aortic Smooth Muscle Responsiveness

When A1 noradrenergic neurons in the caudal ventrolateral medulla of rabbits are destroyed electrolytically or by local injection of the neurotoxin kainic acid, the concentration of vasopressin in plasma increases, causing hypertension. The A1 neurons may tonically inhibit the activity of vasopressin-secreting neuroendocrine cells through a direct hypothalamic projection.

Destruction of noradrenergic neurons in rabbit brainstem elevates plasma vasopressin, causing hypertension

A physiologically based biokinetic model for cesium in the human body.

Renal plasma flow (RPF), glomerular filtration rate (GFR), arginine vasopressin in plasma (AVP), free water clearance (CH2O) and blood pressure (BP) were determined in 11 patients with essential hypertension at the end of 3 consecutive periods of observation each of 6 of weeks duration; indapamide 2.5 mg daily was given in period 2 and placebo in periods 1 and 3. RPF and GFR were reduced by 9% and BP by 9%/14% supine and 14%/12% standing during indapamide treatment. Changes in renal haemodynamics were not correlated with those in BP. AVP was not significantly altered by indapamide and was not correlated with BP. Indapamide reduced CH2O possibly due to the reduction in GFR. It is concluded that indapamide evidently induces redistribution of the cardiac output, with enhanced muscle blood flow and reduced renal perfusion, and that AVP does not seem to be involved in blood pressure regulation in mild to moderate essential hypertension under basal conditions.

Effect of indapamide on renal plasma flow, glomerular filtration rate and arginine vasopressin in plasma in essential hypertension.

Hemodynamic effects of infused arginine vasopressin in congestive heart failure.

SUMMARY The goal of this study was to compare adrenergic neurotransmlssion in isolated vascular smooth muscle from spontaneously hypertensive (SHR) and normotensive rats. Tail arteries, excised from adult SHR and normotensive rats, were cut helically into strips that were mounted in organ chambers between two platinum wire electrodes; isometric contractions were recorded. Vascular responsiveness was determined before and after acute denerration with 6-hydroxydopamine or before and after treatment with phentolamine. Release or displacement of endogenous norepinepbrine was obtained with electrical stimulation, tyramine, and potassium. The sensitivity to exogenous noreplnephrine of innervated vessels was similar for SHR and normotensive rats. Denerration produced a significant shift to tbe left in the concentration-response curve to noreplnephrine only in SHR vessels. Contractile responses to electrical stimulation, tyramine, and potassium were similar in both groups before denervation. Contractile responses to potassium-free solution were greater in SHR than in normotensive vessels. Following denerration, the SHR and normotensive vessels responded similarly to these latter interventions. Blockade of alpha-adrenoceptors with phentolamine reduced contractile responses to all agents in innervated and denerrated vessels. Cocaine caused a slowing of the relaxation following contraction induced by electrical stimulation in both SHR and normotensive vessels. The relaxation of SHR vessels was less affected by cocaine than in normotensive vessels. The tissue content of norepinephrine was similar in SHR and normotensive arterial strips. In arterial strips from SHR the uptake of 'H-norepinephrine was significantly larger than in those from normotensive rats. The results suggest that the reactivity of innervated blood vessels to $$ norepinephrine is similar in SHR and normotensive rats. Important differences in sensitivity to norepinephrine in hypertensive vessels are unmasked when tbe relationship between the vascular smooth muscle cell and the adrenergic nerve terminal is altered. Apparently, the adrenergic nerve terminals in hypertensive blood vessels can modulate the junctional concentration of norepinephrine so that the contractile response to this agent is similar to that in normotensive blood vessels.

Adrenergic neurotransmission in vascular smooth muscle from spontaneously hypertensive rats.

Experiments were performed to determine the monovalent ion specificity of the electrogenic sodium pump in vascular smooth muscle. Helical strips of rat tail artery relaxed in response to potassium after contraction induced by norepinephrine in potassium-free solution. This relaxation is due to the electrogenic pumping of sodium and potassium which produces membrane hyperpolarization. The magnitude of the relaxation was decreased when the strips were incubated in solutions containing low concentrations of potassium (0.01-5.0 mM) instead of zero potassium. Potassium-induced relaxation was inhibited by ouabain. Helical strips also relaxed in response to rubidium, cesium, and ammonium when these were added instead of potassium to a potassium-free solution. The effectiveness of the monovalent ions in producing relaxation was in the following order: rubidium ≥ potassium > ammonium > cesium. Ouabain inhibited the relaxation responses induced by these latter ions. The results suggest: (i) small changes of...

Monovalent Ion Specificity of the Electrogenic Sodium Pump in Vascular Smooth Muscle

Abstract The current study investigates the mechanism by which the concentration of activator Ca2+ is decreased during potassium induced relaxation of vascular smooth muscle. Helically cut strips of rat tail artery were mounted between a fixed base and force transducers; isometric contractions were recorded. The arterial strips relaxed in response to potassium after contraction induced by norepinephrine in potassium-free solution. The efflux of 45Ca2+ from the strips was stimulated by norepinephrine during the potassium-free cycle. This increase in efflux was prevented during potassium induced relaxation. D-600, an inhibitor of transmembrane Ca2+ flux, reduced the magnitude of potassium induced relaxation by 35%. These observations suggest that relaxation in response to potassium is the result of a decrease in membrane permeability to Ca2+ coupled with an increase in Ca2+ sequestration at intracellular sites.

PM Vanhoutte

Papers

Adrenergic neurotransmission in vascular smooth muscle from spontaneously hypertensive rats.

Monovalent Ion Specificity of the Electrogenic Sodium Pump in Vascular Smooth Muscle

Calcium efflux in rat tail artery during potassium induced relaxation.