ArticleBritish journal of pharmacology1993
Quinapril treatment and arterial smooth muscle responses in spontaneously hypertensive rats.
Article in British journal of pharmacology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 38 citations in OpenAlex.
- Quinapril. A reappraisal of its pharmacology and therapeutic efficacy in cardiovascular disorders.Drugs · 1994Trial
- Antihypertensive Potential of Japanese Quail (Biology · 2024Article
- The effects of anti-hypertensive therapy on the structural, mechanical and metabolic properties of the rat aorta.Journal of muscle research and cell motility · 2000Article
- Effect of celiprolol therapy on arterial dilatation in experimental hypertension.British journal of pharmacology · 1996Article
- Dietary calcium and magnesium supplements in spontaneously hypertensive rats and isolated arterial reactivity.British journal of pharmacology · 1995Article
- Endothelial function in spontaneously hypertensive rats: influence of quinapril treatment.British journal of pharmacology · 1995Article
- Effects of enalapril and hydrochlorothiazide on the salt-induced cardiac and renal hypertrophy in normotensive rats.Naunyn-Schmiedeberg's archives of pharmacology · 1994Article
- Enhancement of arterial relaxation by long-term atenolol treatment in spontaneously hypertensive rats.British journal of pharmacology · 1994Article
- Arterial contractions induced by cumulative addition of calcium in hypertensive and normotensive rats: influence of endothelium.Naunyn-Schmiedeberg's archives of pharmacology · 1994Article
- Replacement of salt by a novel potassium- and magnesium-enriched salt alternative improves the cardiovascular effects of ramipril.British journal of pharmacology · 1994Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1 The effects of long-term angiotensin-converting enzyme inhibition with quinapril on arterial function were studied in spontaneously hypertensive rats, Wistar-Kyoto rats serving as normotensive controls. 2 Adult hypertensive animals were treated with quinapril (10 mg kg-1 day-1) for 15 weeks, which reduced their blood pressure and the concentrations of atrial natriuretic peptide in plasma and ventricular tissue to a level comparable with that in normotensive rats. 3 Responses of mesenteric arterial rings in vitro were examined at the end of the study. Compared with normotensive and untreated hypertensive rats, responses to noradrenaline were attenuated in hypertensive animals on quinapril, both force of contraction and sensitivity being reduced. Quinapril also attenuated maximal contractions but not sensitivity to potassium chloride. Nifedipine less effectively inhibited vascular contractions in normotensive and quinapril-treated than in untreated hypertensive rats. 4 Arterial relaxation responses by endothelium-dependent (acetylcholine) and endothelium-independent (sodium nitrite, isoprenaline) mechanisms were similar in normotensive and quinapril-treated rats and more pronounced than in untreated hypertensive rats. 5 Cell membrane permeability to ions was evaluated by means of potassium-free solution-induced contractions of endothelium-denuded denervated arterial rings. These responses were comparable in normotensive and quinapril-treated rats and less marked than in untreated hypertensive rats. 6 Intracellular free calcium concentrations in platelets and lymphocytes, measured by the fluorescent indicator quin-2, were similar in normotensive and quinapril-treated rats and lower than in untreated hypertensive rats. 7 In conclusion, quinapril treatment improved relaxation responses and attenuated contractions in arterial smooth muscle of hypertensive rats. These changes may be explained by diminished cytosolic free calcium concentration, reduced cell membrane permeability, and alterations in dihydropyridine-sensitive calcium channels following long-term angiotensin-converting enzyme inhibition.
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