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Biomedical subjects

D K Chan

Publications and source records attributed to D K Chan.

At least 55 records · Page 3Linked to original sources
PubMed1976

The caudal neurosecretory system. A critical evaluation of the two-hormone hypothesis.

Recent information on the caudal neurosecretory system (urophysis) is collated, with special reference to cellular biology including neural relations, activity and chemistry 8 the biological principles associated with the urophysis, pharmacological analysis of the receptors for these principles, and their possible functions in a physiological sense. The existence of at least two principles, urotensins I and II, is well established. They differ pharmacologically and chemically and may arise from different cell types. At present, osmoregulation, cardiovascular regulation and reproduction are the most likely aspects of organismal physiology wherein these principles may be involved.

Animals↗
PubMed1976

The effects of acetylcholine, biogenic amines and other vasoactive agents on the cardiovascular functions of the Eel, Anguilla japonica.

The blood pressure in the cardinal vein, cardiac chambers and ventral and dorsal aortae have been recorded from conscious eels in water. At low doses, acetylcholine reduced the heart rate but increased the transbranchial differential blood pressure. The effects were abolished by atropine but not by tubocurarine. At doses in excess of 0.1 mug/kg, a secondary rise in arterial blood pressure was observed which could be abolished by bretylium, phentolamine or phenoxybenzamine. Catecholamines did not affect the heart rate although a transient bradycardia due to reflex inhibition could be observed with adrenaline and noradrenaline. Catecholamines increased the cardiac contractile force through an alpha-adrenergic mechanism which was blocked by phentolamine but not by propranolol. The relative potency was noradrenaline greater than adrenaline greater than isoprenaline. A beta-adrenergic receptor located in the branchial circulation led to vasodilation and decrease in transbranchial differential pressure. Both alpha-(vasoconstriction) and beta-(vasodilation) adrenergic receptors were present in the systemic circulation. Dopamine, 5-HT, GABA and bradykinin caused bradycardia abolishable by vagotomy or atropine treatment. Angiotensin II was hypertensive but did not affect the heart rate nor the transbranchial differential pressure. Tyramine caused release of endogenous catecholamines. With repeated doses, tachyphylaxis to the drug was observed. Histamine was without any obvious cardiovascular effects in the eel.

Acetylcholine↗
PubMed1975

Pharmacological effects of urotensins. I. Regional vascular effects of urotensins I and II in the rat.

The effects of urotensins I and II were studied on blood space and inulin space (with 51Cr-labelled erythrocytes and 14C inulin) in organs obtained from rats anaesthetized with pentobarbital. The findings were matched with the effects of urotensins on blood pressure and on perfusion pressure in the isolated perfused rat hind limb (skeletal muscle), intestine, kidney, and lung. Blood space was greatly increased by urotensin I (50 mU/100 g body wt iv) in skeletal muscle, intestine (ileum), ear, renal cortex, medulla and papilla and in adrenal gland, but was decreased in liver and spleen. Blood space changes in these organs run in parallel with the blood-pressure-lowering effect of I. After urotensin II, no significant changes were observed in the above organs, with the exception of the renal cortex where an increase in blood space occurred. Urotensin I caused an increase in inulin space in skeletal muscle, intestine, diaphragm and adrenal, but mobilized extracellular fluid from liver, lung, spleen and ear. In the kidney, urotensin I increased the tissue/plasma inulin ratio in renal cortex, medulla and papilla, indicating water reabsorption. It is concluded that the blood-pressure-lowering effect of urotensin I in the rat is due to a potent vasodilatatory action, mainly exerted in skeletal muscle, mesenteric region, skin and kidney.

Animals↗
PubMed1975

Pharmacological effects of urotensins. II. Renal effects of urotensin I in the rat.

Urotensin I decreased urine flow, glomerular filtration rate and renal plasma flow in intact and hypophysectomized rats. The antidiuretic effect of urotensin I differed from the that caused by AVT in that (a) the urine conductivity was not usually increased by the former, and (b) the rates of excretion of Na and K were different. The use of hypophysectomized rats and of Na-thioglycollate-treated urotensin I preparations indicated that the antidiuretic effect of urotensin I was not due to the release of endogenous ADH, nor was it caused by presence of AVT in the urotensin I samples.

Aminohippuric Acids↗