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Results for “VASOMOTOR SYSTEM”

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At least 307 records · Page 17Linked to original sources
PubMed1977

Bufuralol, a new beta-adrenoceptor blocking agent in a series of benzofuran-2-ethanolamines. Part 2: pharmacology.

1-(7-Ethylbenzofuran-2-yl)-2-tert.-butylamino-1-hydroxyethane hydrochloride (bufuralol) is a non-selective beta-adrenoceptor blocking agent which closely resembles propranolol in its properties, including potency. Bufuralol is devoid of alpha-adrenoceptor blocking activity but possesses beta-adrenoceptor agonist activity. beta-Adrenoceptor blocking activity resides mainly in the (-)-isomer though membrane stabilising properties are associated with both optical isomers.

Adipose Tissue↗
PubMed1979

[Effect of blockade of the adrenergic structures of the hypothalamus on thermoregulatory reactions].

The blockade of alpha-adrenergic receptors of medial preoptic area detained the appearance of vascular thermoregulatory reaction and increased the threshold of the organism central temperature. The blockade of beta-adrenergic structures induced opposite effects. The excitatory efferent impulses from the thermosensitive neurons of the hypothalamus to thermogenic effectors and to the vasomotor system seem to be realized through the alpha-adrenergic structures of the brain, and the inhibitory--through the beta-adrenergic structures.

Animals↗
PubMedDate not supplied

The effects of pathophysiologic state on the metabolism of vasoactive peptides by mammalian lung.

The pulmonary circulation plays a major role in the metabolism of angiotensin I (AI) and bradykinin through the activity of endothelial cell membrane-bound dipeptidylcarboxypeptidase, converting enzyme of kininase II. This report describes studies which investigate the effects of hypoxia on the function of converting enzyme in vivo in dogs and in endothelial cells in culture. Pulmonary converting enzyme function was assessed by both a blood pressure response technique and radioimmunoassay of bradykinin. Conversion of AI in vivo is decreased during acute alveolar hypoxia. At a PaO2 of 30 mmHg, conversion of AI is decreased to one-half control values. This decrease in AI conversion could not be related to hemodynamic factors in the pulmonary vasculature induced by hypoxia. Clearance of bradykinin by lung converting enzyme decreased from 96% at PaO2 levels above 95 torr to 0% below 26 torr. Hypoxic inhibition of enzyme activity was rapid in onset (less than 2 min), was closely correlated with PaO2 (r = 0.92, p less than 0.001) and reversible within 2 min after return to room air breathing. Converting enzyme activity of the systemic vascular bed also is inhibited by hypoxia. Converting enzyme activity also was studied by adding bradykinin or AI to endothelial cells in culture flasks and measuring residual peptide over time by radioimmunoassay. Hypoxia rapidly (less than 2 min) decreased enzyme activity and room air restored it rapidly. There was no enzyme activity below a PO2 of 30 mmHg. Hypoxia does not affect the activity of purified converting enzyme free of the endothelial cell. Metabolic and respiratory acidosis, as well as metabolic and respiratory alkalosis, had no significant effect on converting enzyme function in vivo in intact animals. While converting enzyme is resistant to a number of pathophysiological insults, it is extraordinarily responsive to acute hypoxia which may have important implications for systemic vasomotor control in conditions associated with clinical hypoxia and hypoxemia.

Acid-Base Equilibrium↗
PubMed1978

How vascular smooth muscle works.

Electrical recordings made from vascular smooth muscle during the last 15 years make it clear that the role of electrical activity in controlling contraction is often important but varies greatly both between different vessels and for different responses of a given vessel. Only a few mammalian vessels have widely conducted electrical activity, but others can develop this activity, with consequent rhythmical contraction, when made anoxic and stimulated. Action potentials play a part in smooth non-rhythmical responses of arteries to nerves and hormones, while passive conduction of depolarization round the vessel wall is responsible for ring contractions of arteries after local injury. Ca and K cause vasodilatation largely by hyperpolarizing the smooth muscle cells. Electrical activity plays no part in some responses. In particular noradrenaline can contract arteries by directly promoting entry of extracellular Ca, and also by releasing Ca stores by non-electrical means. These processes are particularly important in the inner muscle of arteries, which is not directly innervated.

Action Potentials↗