PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Pressoreceptors”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1977

Analysis of bladder configuration and pressure from pressoreceptor stimulation in rabbits.

In a previous study (Bödeker, J., Vogt, W., Kölln, C.-P., and Nagel, R.: Invest. Urol., 12: 461, 1975.) pressoreceptor stimulation induced micturition at less than normal bladder filling. Furthermore, urethral pressure profile decreased in both maximal and mean values. In the present investigation the effects of pressoreceptor stimulation on bladder configuration, intravesical pressure, and vesicoureteral reflux were studied. With pressoreceptor stimulation, the bladder outlet became more funnel-shaped; the change in bladder configuration occurred without alteration in intravesical pressure; and vesicoureteral reflux could not be demonstrated.

Animals↗
PubMedDate not supplied

Effect of carotid pressoreceptor stimulation on integrated systemic venous bed.

In 9 mongrel dogs, venous return was completely drained from the caval veins to an oxygenator and returned to the femoral arteries with a roller pump. Perfusion rate of systemic circulation and blood pressures in both caval veins were kept constant. Changes in the oxygenator weight were recorded and reflected reciprocal changes in integrated systemic venous blood volume. The vagal nerves were dissected. The carotid sinuses were separately perfused with blood by means of a pump. In 25 experiments, increases in carotid sinus pressure of 15 to 74 mm Hg resulted in decreases in systemic arterial pressure of 10 to 57 mm Hg and increases in systemic venous blood volume of 1.1 to 4.7 ml/kg. On an average, systemic venous blood volume was changed by 1.25 +/- 0.08 ml/kg when the change in systemic arterial pressure was 10 mm Hg. It is concluded that the carotid sinus pressoreceptor reflex considerably alters the systemic venous capacity which in tern alters venous return and cardiac output. These changes in cardiac output are expected to be small, but sufficient to alter the arterial pressure considerably. Thus, they might contribute nearly as much as the reflex effect on total peripheral resistance to the reflex control of arterial pressure.

Animals↗
PubMed1976

Cardiac pressoreceptors and peripheral resistance.

The results obtained show that the pressoreceptors, probably ubicated in the left ventricle of the rat, respond to the distention with vasodilatation. The afferent tract of this reflex is in the vagus nerve and the efferent one is in the sympathetic nervous system. The probable function of this reflex is discussed.

Animals↗
PubMed1977

Afferent discharges from venous pressoreceptors in liver.

Afterent discharges were observed in dissected filaments or single nerve fibers of hepatic nerve in the guinea pig and the rabbit. Increasing the perfusion pressure of the portal vein in isolated liver preparation in the guinea pig caused an increase in afferent discharge rate. Discharge patterns were compatible with those of the slowly adapting type. Increasing the portal venous pressure by means of intravenous injection of Locke's solution into the left jugular vein in the rabbit in vivo caused an increase in afferent discharge rate. Increasing the hepatic arterial pressure was without effect. It is suggested that pressoreceptors are present in or near the venous wall of the portal venous system and that they send information about blood pressure in the portal vein to the central nervous system.

Action Potentials↗
PubMed1976

Electron microscopic studies of the pressoreceptor fields of the carotid sinus of the dog.

In the dog, pressosensitive endings of the sinus nerve extend along the border between the adventitia and media of the carotid sinus wall. The axon endings, containing a great number of mitochondria, can be divided into small (600-2,000 nm) and large (6,000-8,000 nm) end swellings. In the terminal region the pressosensitive fibers are surrounded by ramified and highly structured Schwann "terminal cells". The topographic location in relation to elastic and collagenous tissue indicates a functional connection between receptors and efferent nerve endings in the immediate surroundings has been discussed in this report. Several axon endings contain variable amounts of glycogen which is regarded as an indication for the inactive metabolic state of the ending. Axonal swellings demonstrate considerable modification in structure, such as loss of structural integrity in mitochondria, the formation of lamellar fields, vesicular irregularities and disintegration of axoplasm, all of which are considered as the morphological expression of "wearing out", degeneration and possibly regeneration.

Animals↗
PubMed1978

A mechanism to explain the antihypertensive action of propranolol.

The present experiments were designed to measure the direct effects of propranolol on carotid sinus pressoreceptor nerve activity in the semi-isolated, superfused sinus of the cat. Propranolol (5 microgram/ml) significantly enhanced carotid sinus nerve activity at perfusion pressures of 100, 150 and 250 mm Hg. The enhancement was due primarily to the recruitment of new fibers. In similar preparations, perfused at constant flow, propranolol increased sinus resistance in parallel with the increase in sinus discharge. These effects were rapidly dissipated by rinsing with drug-free perfusion solution. The evidence suggests that propranolol may produce a change in either the elastic or autoregulatory modalities of sinus smooth muscle. This may produce a functional "resetting" of the sinus and provide a mechanism to explain the antihypertensive effect of propranolol.

Action Potentials↗
PubMed1977

Effect of beta adrenoceptor antagonists on baroreceptor reflex sensitivity in hypertension.

High-pressure baroreceptor reflex sensitivity (BRS) was estimated by measuring the reflex heart rate response to pharmacologic elevation of blood pressure (phenylephrine, 150 to 200 microgram intravenously) in 18 patients with essential hypertension on two occasions: after a 4-wk placebo period and after 9 wk of incremental doses of oral timolol (20, 40, and 60 mg daily). On placebo, measurements were performed both before and after propranolol (0.2 mg/kg intravenously). The level of cardiac vagal inhibition, estimated by the heart rate change after atropine (0.04 mg/kg intravenously), was similar in placebo and on timolol, thereby permitting comparisons of BRS. BRS on placebo (before and after propranolol) correlated with BRS on timolol ( r = 0.87 and 0.90, p less than 0.001), attesting to the reproducibility of BRS measurements. BRS was unchanged by either short-term (propranolol) or long-term (timolol) beta adrenoceptor inhibition. Results were similar in responders (n = 10), whose mean arterial blood pressure on timolol fell by 10 mm Hg or more, and in nonresponders. The findings do not provide evidence for a change in gain of the baroreceptor reflex arc under conditions of short- or long-term beta adrenoceptor inhibition.

Adult↗
PubMed1979

Effect of alpha-methyldopa on cardiac output in hypertension.

Hemodynamic and blood volume changes, systolic time intervals, and baroreflex mechanisms were studied in 20 patients with hypertension after methyldopa (12 +/- 0.9 mg/kg/day). The drug was administered orally during 7 days' hospitalization on a normal sodium diet (110 mEq/day). There was a fall in blood pressure and in total peripheral resistance, without significant change in cardiac index, heart rate, and stroke index. There were increases in plasma and blood volume (p less than 0.05) but no change in cardiopulmonary blood volume or systolic time intervals. The unchanged heart rate was associated with an increased sensitivity ( less than 0.05) of the baroreflex mechanisms. The study supports the view that the unchanged cardiac output after methyldopa is related to important changes in control of cardiac output, including redistribution of blood volume and modifications in baroreflex mechanisms.

Adult↗
PubMedDate not supplied

Circulatory effects of diazepam in heart disease.

Diazepam was administered to ten patients with heart disease during diagnostic cardiac catheterization, in order to determine whether or not this drug's circulatory actions could alter results obtained during the procedure. Diazepam produced no change in baroreceptor sensitivity; however, there was a significant rise in heart rate and a significant fall in aortic systolic and left ventricular end-diastolic pressures. Cardiac index was unchanged, whereas stroke volume fell significantly. Systemic vascular resistance and peak left ventricular dp/dt did not change throughout the study. Clinical response in terms of sedation was judged to be satisfactory in eight patients, and no adverse effect on respiration was noted. Diazepam has little effect on basal circulatory and respiratory parameters when changes in these parameters are averaged for our ten patients. However, substantial changes in hemodynamic parameters did occur in several individuals, and such alteration in circulatory function must be considered when this agent is used routinely in patients having diagnostic cardiac catheterization.

Blood Pressure↗