Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several theoretical considerations suggest that potentiation of central norepinephrine mechanisms may improve motor performance in patients with Parkinson disease receiving concurrent treatment with levodopa. Clonidine hydrochloride, an antihypertensive drug believed to directly stimulate brain norepinephrine receptors, was administered to a group of patients with relatively mild Parkinson disease and coexisting essential hypertension and to three patients with Parkinson disease manifesting the "on-off" response to levodopa. Although a significant antihypertensive effect was achieved, a change in parkinsonian disability could not be demonstrated.
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PMID:Clonidine in Parkinson disease. 112 78

The effects of the antihypertensive imidazoline compounds 2-(5 fluor-0-toluidine)-2-imidazoline hydrochloride (ST 600) and 2-(2, 6 dichlorophenylamine)-2-imidazoline hydrochloride (ST 155, clonidine, Catapres) on intra-arterial pressure, cardiac output, stroke volume, heart rate, total peripheral resistance, renal blood flow, glomerular filtration rate, renal vascular resistance, plasma volume, plasma renin and aldosterone concentration were studied in five patients with essential hypertension. The antihypertensive action of both compounds was similar and was accompanied by a reduction in heart rate and in cardiac output, total peripheral resistance being unchanged. There was no significant decrease in renal blood flow and glomerular filtration rate. Plasma volume and plasma concentrations of renin and aldosterone also did not change significantly. In the face of similar reductions in blood pressure, no differences were observed between cardio-renal haemodynamic responses after ST 600 and clonidine. However ST 600 had a longer lasting effect (8-12 hours).
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PMID:Comparison between the effects of ST 600 and clonidine. 119 Sep 9

Clonidine hydrochloride via the central nervous system lowers blood pressure, inhibits ACTH and catecholamine release, and stimulates growth hormone secretion. To evaluate the effect of this drug on the release of glucoregulatory hormones during hypoglycemia, we studied the responses to insulin-induced hypoglycemia (0.1 units/kg) in 10 patients with mild essential hypertension before and after treatment for 16 weeks with transdermal clonidine. Clonidine significantly lowered blood pressure, basal plasma norepinephrine levels, and epinephrine and renin activity but did not affect basal growth hormone concentrations. Clonidine significantly reduced the norepinephrine and epinephrine responses to hypoglycemia (norepinephrine AUC from 207 +/- 16 SE to 156 +/- 25 nmol/L/min, epinephrine from 157 +/- 28 to 99 +/- 29 nmol/L/min; both p less than 0.05) and increased the growth hormone response (AUC from 763 +/- 148 ng/min/ml to 1164 +/- 292 ng/min/ml; p less than 0.05) but did not affect the cortisol response or the magnitude or rate of glucose recovery from hypoglycemia. Thus transdermal clonidine has several effects on glucose counterregulatory hormones that do not significantly alter insulin sensitivity or impair recovery from hypoglycemia.
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PMID:Effect of transdermal clonidine on the endocrine responses to insulin-induced hypoglycemia in essential hypertension. 264 99