Biomedical subjects

C Rosendorff

Publications and source records attributed to C Rosendorff.

At least 91 records · Page 5Linked to original sources

PubMed1975

Effects of jaundiced plasma on vascular sensitivity to noradrenalin.

Alterations in renal perfusion have been shown in a variety of liver diseases. We have examined the possibility that the syndrome is due to a renal vascular hypersensitivity to noradrenalin (NA). Isolated perfused kidneys and segments of rabbit femoral artery were used. Potentiation of the pressor effects of injected NA occurred in all (five artery and five kidney) preparations when jaundiced baboon plasma was perfused. These changes were significant (P less than 0.05) in nine out of the ten experiments. Controls to which normal baboon plasma was administered showed no such change. No correlation was found between the degree of NA potentiation and the plasma concentrations of bilirubin (total and conjugated), serum glutamic oxaloacetic transaminase, blood urea nitrogen, serum glutamic pyruvic transaminase, alkaline phosphatase, Na+ ions or K+ ions in the jaundiced plasma. Plasma renin levels were not significantly changed. When arteris were perfused with Krebtentiation of NA was found. Perfusion of sodium taurocholate or sodium deoxycholate (400 mug/ml) yielded no potentiation. Thus, the altered renal perfusion associated with jaundice may be attributed to a potentiated pressor response to NA which may be caused by an increased level of cholesterol carried on the beta-lipoprotein.

Animals↗

PubMed1975

The effect of noradrenaline, adrenergic blocking agents, and tyramine on the intrarenal distribution of blood flow in the baboon.

The intrarenal distribution of blood flow in the baboon was measured using the 133xenon clearance technique, and dose-response curves for the various components of renal blood flow were determined during intra-arterial infusions of noradrenaline; the alpha-adrenergic blocking agent, phenoxybenzamine; the beta-adrenergic blocking agent, propranolol; and tyramine which causes the release of endogenous NA. High doses of noradrenaline reduced flow in the outer cortex; this effect was attenuated by phenoxybenzamine, but not by propranolol. Tyramine had no effect. These r results suggest that there are alpha-adrenergic receptors in the resistance vessels of the kidney but are inconsistent with an important role for NA-mediated autonomic control of renal blood flow.

Animals↗

PubMed1975

Adrenoceptors in intracerebral resistance vessels.

1. The effects of tyramine and isoprenaline on hypothalamic blood flow (HBF) were measured in conscious rabbits. 2. Injections of small doses of tyramine caused an increase in HBF while larger doses caused a decrease in HBF. 3. Isoprenaline injections also produced an increase in HBF. 4. The vasodilatation induced by isoprenaline and the small dose of tyramine was blocked by propranolol. 5. The vasoconstriction induced by the larger doses of tyramine was abolished by phenoxybenzamine. 6. Chemical sympathectomy of the hypothalamus with 6-hydroxydopamine and depletion of biogenic amines by reserpine also abolished tyramine-induced vasocoonstriction. 7. These results suggest the presence of alpha- and beta-adrenoceptors in cerebral resistance vessels, and that these receptors may be activated by released (endogenous) noradrenaline.

Animals↗

PubMed1975

The effects of hypercholesterolaemic plasma on vascular sensitivity to noradrenaline.

1. The pressor responses to injected noradrenaline (NA) of 42 isolated perfused femoral arteries of the rabbit were studied. 2. Potentiation of the responses was found when hypercholesterolaemic plasma was perfused through the arteries. No change was found with normal plasma. 3. Potentiation of the responses was found when isolated beta-lipoprotein in Krebs solution was perfused. No change was found with similar amounts of bovine-albumen. 4. Pure cholesterol dissolved directly into normal plasma, and dissolved via propanol into Krebs solution or plasma caused no potentiation. Propanol alone in Krebs or plasma had no effect. 5. Potentiation was caused by a decreased equilibrium coefficient (Keq) for the NA-adrenoceptor interaction and an increased maximal pressor response (Rmax). 6. It is concluded that cholesterol carried on its apoprotein is capable of potentiating the pressor effects of noradrenaline.

Animals↗

PubMed1975

Hypothalamic heating and cooling in monoamine-depleted rabbits.

The role of monoamines in the thermoregulatory responses induced by hypothalamic heating and cooling was investigated in conscious rabbits. Depletion of hypothalamic catecholamines by pretreatment with 6-hydroxydopamine (6-OHDA) greatly attenuated the rectal temperature and vasomotor responses to hypothalamic heating and cooling. Pretreatment with p-chlorophenylalanine (PCPA) depleted the animals of 5-hydroxytryptamine (5-HT). The results obtained are consistent with 5-HT having an inhibitory role in the rabbit's vasomotor response to heat stress and activating heat conservation during cold stress. Reserpinized rabbit were depleted of both norepinephrine (NE) and 5-HT and were found to be unresponsive to hypothalamic temperature changes. We conclude that the integrity of the monoaminergic system is viral for the correct functioning of the hypothalamus in maintaining a constant body temperature.

Animals↗

PubMed1975

Renovascular resistance and noradrenaline.

Stimulation of the renal nerves can cause cortical vasoconstriction either by direct activation of vascular smooth muscle or by the generation of angiotensin II following renin release from the juxtaglomerular cells. High doses ( greater than 5 mug/min) of the renal neurotransmitter noradrenaline (NA) infused into the renal artery of the baboon causes cortical vasoconstriction. This NA-induced vasoconstriction is significantly reduced (P less than 0.001) by SQ20881, an inhibitor of converting enzyme, and by saralasin, a competitive inhibitor of angiotensin II. These results suggest that NA stimulates the renin-angiotensin mechanism. The further addition of the alpha-adrenergic blocking agent, phenoxybenzamine, to the NA-SQ20881 or NA-saralasin infusate completely abolishes NA-induced cortical vasoconstriction. These results suggest that NA-induced cortical vasoconstriction in the kidney is mediated by activation of both the renin-angiotensin system and alpha-adrenergic receptors.

Angiotensin II↗

PubMed1975