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M V Conde

Publications and source records attributed to M V Conde.

22 records · Page 2Linked to original sources
PubMed1978

Adrenergic vasoconstriction of the goat middle cerebral artery.

The effects of field electrical stimulation on the contractile response of the isolated middle cerebral artery of the goat were evaluated before and after the use of experimental procedures designed to test the adrenergic component involved. Supramaximal stimuli produced frequency-dependent increases in tension. This response was significantly reduced by phentolamine (10(-6) M), tetrodotoxin (3 X 10(-6) M), and bretylium (5 X 10(-5) M), but not by cocaine (10(-6) M). Arterial segments from goats pretreated with reserpine and from goats in which both superior cervical sympathetic ganglia had been removed 12 days prior to the experiment also showed a significant decrease in the contraction elicited by electrical stimulation. The norepinephrine concentration of the arteries of the circle of Willis from control goats was 2.10 microgram per gram of tissue. Reserpine or gangliectomy reduced the catecholamine content to undetectable levels. It is likely that a major part of the contractile response of cerebral arteries to electrical stimulation is due to release of endogenous norepinephrine which in turn activates the alpha-adrenergic receptors.

Animals↗
PubMedDate not supplied

Heterogeneity of endothelium-dependent mechanisms in different rabbit arteries.

The possible endothelial factors involved in endothelium-dependent relaxations induced by acetylcholine (ACh) in aorta, mesenteric and femoral arteries of rabbit were analyzed. In thoracic aorta precontracted with noradrenaline, NG-nitro-L-arginine methyl ester (L-NAME) and methylene blue (MB), inhibitors of nitric oxide (NO) synthase and guanylate cyclase, practically abolished ACh relaxation. This relaxation was reduced by the Na+ pump inhibition with ouabain and K(+)-free solution, and by the blockade of Ca(2+)-dependent K+ channels with tetraethylammonium (TEA). Ouabain reduced the relaxation produced by the NO donor, sodium nitroprusside (SNP). In the mesenteric artery, L-NAME and MB produced a small reduction of ACh relaxation. However, ouabain, K(+)-free medium and TEA markedly decreased this relaxation. SNP induced a relaxation which was diminished by ouabain. In segments precontracted with high K+, ACh relaxation was abolished by L-NAME and MB. In femoral arteries, L-NAME and MB reduced ACh relaxation. The stimulated cGMP concentrations caused by ACh or SNP were less in the aorta than in mesenteric and femoral arteries. These results suggest that ACh relaxation is mediated: in aorta by endothelial NO which may hyperpolarize to some extent the smooth muscle cells through the sodium pump activation, in mesenteric artery by endothelium-derived hyperpolarizing factor and NO, the latter being clearly expressed in segments contracted with high K+, and in femoral artery essentially by endothelial NO release.

Acetylcholine↗
PubMedDate not supplied

In vivo and In vitro studies on the cerebrovascular dilatation induced by diazoxide in normotensive and renal hypertensive goats.

We studied the in vivo and in vitro effects of diazoxide on the cerebral circulation of 8 normotensive (mean arterial pressure = 100 mm Hg) and 5 renal hypertensive (mean arterial pressure = 146 mm Hg) goats. Injections of diazoxide (0.3-27 mg) into the internal maxillary artery of unanesthetized goats produced dose-dependent increases in cerebral blood flow (electromagnetic flowmeter), this effect being significantly higher in hypertensive goats. Intravenous injection of 5 mg/kg of diazoxide into normotensive goats increased cerebral blood flow 40 ml/min/100 g and mean arterial pressure dropped 22 mm Hg whereas in hypertensive goats cerebral blood flow was unchanged and mean arterial pressure decreased 50 mm Hg. The increase in heart rate due to intravenous diazoxide was similar in normotensive and hypertensive goats (35 beats/min). Cumulative applications of diazoxide (10(-5) to 10(-3)M) on isolated middle cerebral arteries produced dilatory responses both under resting conditions and after previous tonic contraction by serotonin. This relaxation was significantly greater in arterial segments from hypertensive goats. The results indicate that diazoxide exerts powerful dilatatory effects on cerebral vessels, both in vivo and in vitro, and that these effects are particularly evident in hypertensive animals.

Animals↗