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Biomedical subjects

C Rosendorff

Publications and source records attributed to C Rosendorff.

At least 37 records · Page 2Linked to original sources
PubMed1991

Angiotensin II induced phosphorylation of myosin light chain in vascular smooth muscle cells from spontaneously hypertensive and normotensive rats.

STUDY OBJECTIVE: The aim was to determine the changes in the phosphorylation of myosin light chain induced by angiotensin II in cultured vascular smooth muscle cells derived from normotensive (WKY) and spontaneously hypertensive rats (SHR). DESIGN: Extracts of vascular smooth muscle cells incubated with [32P]orthophosphoric acid were subjected to 4M urea-SDS electrophoresis, followed by autoradiography and laser densitometry. EXPERIMENTAL MATERIAL: Confluent primary cultures of vascular smooth muscle cells from aorta, superior mesenteric arteries and cerebral arteries were used. MEASUREMENTS AND MAIN RESULTS: The basal myosin light chain phosphorylation of SHR did not differ significantly from that of WKY. Stimulation with 1 nM angiotensin II increased incorporation of 32P into the myosin light chain, which peaked at 4 min and then slowly declined until 15 min. Exposure to angiotensin II (0.001-10 nM) for 4 min evoked a dose dependent increase in the phosphorylation of myosin light chain with a maximal response 40-45% above basal values. No significant differences in the response to angiotensin II were detected between cells derived from the two strains. Saralasin, a specific angiotensin II antagonist, did not affect the basal phosphorylation of myosin light chain but completely abolished the effect of angiotensin II. CONCLUSIONS: Angiotensin II enhances the phosphorylation of the myosin light chain from vascular smooth muscle cells in aorta, mesenteric arteries, and cerebral arteries, but there are no differences in response between SHR and WKY.

Angiotensin II↗
PubMed1990

Differential size distribution of atrial dense granules in spontaneously hypertensive, Wistar-Kyoto and Wistar rats.

The differential size distribution of atrial dense granules (ADGs) in spontaneously hypertensive rats (SHR) and two normotensive controls, Wistar and Wistar-Kyoto (WKY) rats, was investigated. The ADGs in SHR were smaller than those in Wistar rats. The ADGs of WKY rats were of intermediate size. It is possible that ADGs are more rapidly secreted in SHR compared with WKY and Wistar rats or that the smaller-diameter granules may contain more atriopeptinogen than the larger granules. The intermediate size of the ADGs in WKY suggests that the WKY variant is morphologically intermediate between the SHR and Wistar strains.

Animals↗
PubMed1988

Effects of angiotensin converting enzyme inhibition and beta-blockade on exercise responses in hypertensive patients.

We compared exercise responses in two groups of hypertensive patients treated with an angiotensin converting enzyme (ACE) inhibitor (lisinopril, 20-80 mg/day, n = 17) or a cardioselective beta-blocker (atenolol, 50-200 mg/day, n = 9). Measurements were made at rest and during exercise at 25 W (2.7 mets) and at 50 W (3.8 mets) on a bicycle ergometer (where mets is exercising oxygen consumption/resting oxygen consumption) after 4 weeks of placebo, and again after 12 weeks of drug administration. Both drugs reduced (P less than 0.05) mean arterial pressure. Atenolol caused significant decreases in the heart rate (approximately 25%) and cardiac output (approximately 26%; Defares CO2 rebreathing), and significant increases in total peripheral resistance (approximately 30%) and arteriovenous O2 content (approximately 20%). Lisinopril decreased (P less than 0.05) stroke volume. At the same exercise intensity systolic blood pressure, arteriovenous O2 and total peripheral resistance were lower (P less than 0.05) and the heart rate was higher (P less than 0.05) after lisinopril than after atenolol. After the treatment of hypertension with the ACE inhibitor the responses to exercise were less restrictive than those after treatment with the cardioselective beta-blocker.

Atenolol↗
PubMed1988

Age dependence of the pressor sensitivity to noradrenaline and angiotensin II during calcium channel blockade in hypertensive patients.

We investigated the hypothesis that at least part of the vasopressor activity of noradrenaline (NA) and angiotensin II (Ang II) in humans is due to the activation of receptor-dependent calcium channels. Thirty patients (15 aged 50-65 years and 15 aged 66-80 years) with diastolic blood pressure of 95-120 mm Hg were given placebo (P) for 4 weeks, and then nitrendipine (N) 20-40 mg/day for 12 weeks. After 4 weeks on placebo, and again after 12 weeks on nitrendipine, NA 40, 80, 160, and 320 ng/kg/min, followed by Ang II 2.5, 5, and 10 ng/kg/min, was infused intravenously, and steady state systolic, diastolic, and mean arterial blood pressure and heart rate were measured. Older patients were found to be significantly less sensitive than younger patients to the pressor effects of NA. N decreased NA sensitivity, more in younger than older patients. Older patients were significantly more sensitive than younger patients to the pressor effects of Ang II. N also decreased Ang II sensitivity, more in older than younger patients. We conclude that at least some of the vasopressor activity of NA and Ang II is due to activation of calcium channels, and that these effects are age dependent.

Aged↗
PubMed1988

Urapidil in the treatment of hypertension.

Urapidil is an alpha 1-adrenoceptor antagonist which also has a central antihypertensive effect, the mechanism of which has yet to be conclusively defined. A number of open and comparative studies have produced evidence for the efficacy and safety of urapidil. A study recently completed by the author produced a dose-dependent antihypertensive effect of urapidil which, however, failed to achieve statistical significance, probably due to a large variance of the data and an unexpectedly large placebo effect. Adverse reactions are those expected from an alpha 1-blocker, particularly dizziness, as well as nausea and fatigue. Urapidil is potentially an important new antihypertensive agent; further variable dose and combination (with other antihypertensive agents) studies would help further define its therapeutic niche.

Adult↗
PubMed1987

Beta-adrenergic receptors and oxygen transport.

We investigated whether stimulation of baboon erythrocyte beta-adrenoreceptors affects oxygen transport by haemoglobin. To assess oxygen transport we measured the PO2 at which the haemoglobin was 50% saturated (P50) and the Hill parameter 'n'. Blood at PO2s ranging from 10 to 90 mm Hg was exposed to a 10(-3) M concentration of the agonists l-isoproterenol, l-epinephrine and l-norepinephrine in the presence and absence of 10(-5) M dl-propranolol. None of the adrenergic agents which were used in these experiments produced significant changes in either 'n' or P50 and the concentrations of 2,3-diphosphoglycerate and lactate were not altered by the agonists. We conclude from these results that short-term adrenergic stimulation of the baboon erythrocyte beta-adrenoreceptor does not affect factors known to influence oxygen transport, oxygen delivery or haemoglobin itself.

2,3-Diphosphoglycerate↗
PubMed1986

Indoramin in the hypertensive patient with concomitant disease: clinical experience.

Hypertension has a high prevalence in most countries, so it is to be expected that hypertension will be found together with other common diseases in many patients. The association between the hypertension and the concomitant disease may be causal or casual. The presence of some other disease in the hypertensive patient often places severe restraints on the choice of antihypertensive therapy. Indoramin, an alpha adrenoreceptor antagonist may be used without ill-effect in the therapy of hypertension in patients who also have chronic obstructive airways disease, congestive heart failure, mild renal failure, peripheral vascular disease, angina pectoris, and diabetes mellitus. In at least some of these patients, the use of beta adrenoreceptor blocking drugs or thiazide diuretics would be contraindicated. We do not know whether these advantages of indoramin are unique or whether they are a general property of all alpha-adrenoreceptor antagonists.

Angina Pectoris↗
PubMed1986

Alpha-adrenoreceptors in hypertension.

The most important central autonomic pathways in the control of arterial blood pressure are the baroreceptor reflex pathway and descending pathways from the hypothalamus. Central neurotransmitters in these pathways are L-glutamate, substance P, norepinephrine (NE), gamma-aminobutyric acid, epinephrine, neuropeptide Y, and acetylcholine. At peripheral autonomic neurovascular junctions, there are prejunctional alpha 2- and dopamine-2 receptors, which inhibit NE release, and beta- and serotonin receptors, which stimulate NE release. Postjunctional alpha 1-receptors open sodium channels, open calcium channels via phosphoinositol release, and release intracytoplasmic calcium. Postjunctional alpha 2-receptors, which are extrasynaptic, inhibit adenylate cyclase and also open calcium channels. In animal models of hypertension, changes in alpha-receptor density have been reported. In spontaneously hypertensive rats, increased renal beta- and alpha 2-receptors, respectively, may enhance renin release and cause sodium and water retention. In experimental (renovascular) hypertension, vascular postsynaptic (vasoconstrictor) alpha 1- and alpha 2-receptors are increased. In both models of hypertension, beta-receptors are down-regulated. Selective alpha 1-antagonists, such as indoramin and prazosin, decrease arterial blood pressure by postsynaptic alpha 1-blockade; alpha 2-receptor inhibition of NE release is unaffected so that there is no beta-receptor-mediated tachycardia.

Adrenergic alpha-Agonists↗
PubMed1985

Comparison of the antihypertensive effect of enalapril and propranolol in black South Africans.

Angiotensin-converting enzyme (ACE) inhibitors are useful antihypertensive agents. Enalapril maleate is a new ACE inhibitor with actions similar to those of captopril but with fewer side-effects. A study was conducted on 19 black South Africans with mild or moderate essential hypertension; enalapril was compared with propranolol as monotherapy or together with hydrochlorothiazide in a 1-year randomized, double-blind, parallel study. Neither enalapril nor propranolol alone produced consistent, significant reductions in blood pressure. There were no significant differences between the blood pressure responses to enalapril and to propranolol (either with or without hydrochlorothiazide). It is concluded that neither enalapril nor propranolol is effective as monotherapy in the treatment of hypertension in South African blacks, but that both require the addition of a thiazide diuretic.

Adult↗
PubMed1985

Creatine kinase release not associated with myocardial necrosis after short periods of coronary artery occlusion in conscious baboons.

The effects of 15 minute periods of coronary artery occlusion on plasma creatine kinase (CK) and CK-MB isoenzyme activity, regional myocardial function and subsequent myocardial necrosis were studied in six conscious baboons 2 to 3 weeks after recovery from instrumentation. Mid left anterior descending coronary artery occlusion induced complete loss of systolic wall thickening (ultrasound transit time technique) and decreases in epicardial (-93%) and endocardial (-96%) blood flows (microsphere technique). Reperfusion after 15 minutes resulted in complete recovery of regional function 24 hours later. Serial plasma enzyme activity revealed a significant increase in total CK from 71 +/- 11 to 976 +/- 158 U/liter and in CK-MB from levels that were too low to measure to 21.4 +/- 2.9 U/liter. At autopsy, neither gross pathologic evidence (triphenyltetrazolium chloride staining technique) nor histologic evidence of myocardial necrosis was observed. Thus, in the conscious baboon short episodes of myocardial ischemia are associated with a significant appearance of CK and CK-MB in the blood in the absence of cellular necrosis.

Animals↗