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)

Common carotid blood flow and cold pressor test were evaluated in 16 patients with sustained essential hypertension before and after 30 days treatment with the converting enzyme inhibitor Enalapril (20 mg). Enalapril decreased blood pressure and carotid vascular resistance with no significant change in heart rate. After treatment, despite a wide range of the responses, the changes in systolic blood pressure to cold test were significantly attenuated, whereas the heart rate responses were not. Acute random and double blind administration of either Cadralazine or Nitrendipine, two vasodilating drugs which are known to cause an activation of the autonomic nervous system, were performed before and after long term treatment by Enalapril. Whereas the blood pressure and heart rate responses to cold test was unmodified by these compounds before Enalapril treatment, significant changes were observed after converting enzyme inhibition: Cadralazine reduced the heart rate response whereas Nitrendipine increased it significantly. The study provides evidence that converting enzyme inhibition causes sympatho-inhibitory influences which are principally observed in stress conditions, with heterogeneous responses depending on the nature and the type of stimulation.
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PMID:An indirect evaluation of the effect of the autonomic nervous system following converting enzyme inhibition in hypertension. 139 74

The antihypertensive effects of the hydralazine-related compound cadralazine (2-(3-[6-(2-hydroxypropyl)ethylamino]pyridazinyl)ethyl carbazate, ISF 2469), were investigated in 16 patients with primary hypertension concurrently treated with beta-blockers and diuretics. The protocol included a double-blind placebo controlled haemodynamic evaluation after the first tablet and two 4-week double-blind placebo controlled cross-over periods followed by an open evaluation during 2 months. Cadralazine induced a moderate, prolonged fall in blood pressure that was associated with vasodilatation and slight increases in cardiac output (dye-dilution) and heart rate. Renal plasma flow (PAH) and glomerular filtration rate (51Cr-EDTA) were not significantly influenced, but the filtration fraction was reduced. Plasma concentrations of noradrenaline and adrenaline rose, whereas plasma renin activity was unchanged. The haemodynamic parameters were not correlated with the plasma concentrations of cadralazine. During chronic cadralazine treatment the supine blood pressure was significantly lower than during the double-blind placebo phase (160/93 vs 174/102 mmHg). The compound was generally well tolerated but the body weight increased slightly (1.1 kg), probably because of fluid retention. Several patients who had previously experienced side effects with hydralazine, including one with hydralazine-syndrome, tolerated cadralazine well. This suggests that cadralazine does not cross-react with hydralazine.
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PMID:Acute systemic and renal haemodynamic effects and long-term antihypertensive action of cadralazine in patients pretreated with beta-blockers and diuretics. 288 88

Using pulsed Doppler methods, hemodynamics of the common carotid and the brachial arteries were measured in 10 patients with essential hypertension. After vasodilatation due to Cadralazine, a Dihydralazine-like substance, mean arterial pressure significantly decreased and heart rate increased. Change in PRA was significantly and positively correlated with the change in heart rate. In the brachial artery circulation, diameter and vascular resistance decreased while blood flow velocity and volumic blood flow did not increase significantly. In the common carotid artery circulation, diameter, mean blood flow did not change. However, vascular resistance and tangential tension decreased slightly. The increase in heart rate was strongly and negatively correlated (r = 0.82 p less than 0.01) with the change in the carotid artery tangential tension (measured as the product between mean arterial pressure and arterial radius) while no comparable correlation was observed with the change in blood pressure or arterial radius alone. The study suggested that in essential hypertensives, modifications in the carotid artery tangential tension secondary to arteriolar vasodilatation contribute actively to the baroreflex response.
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PMID:[Non-invasive study of the role of carotid distension in the baroreflex response to the arteriolar vasodilator cadralazine in essential hypertension]. 309 14