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J L Colas

Publications and source records attributed to J L Colas.

12 recordsLinked to original sources
PubMed2000

[Fibrinogen: a cardiovascular risk factor].

AN INDEPENDENT RISK FACTOR: Pathophysiological and epidemiological data show that fibrinogen is an independent risk factor for atherosclerosis with a synergistic effect on classical risk factors. CORONARY ARTERIES: Serum fibrinogen level is an independent predictor of the presence and severity of atheromatous lesions of the coronary arteries. It is also predictive of coronary events such as sudden death, myocardial infarction or angina pectoris. OTHER VESSELS: Fibrinogen is also a marker of cerebrovascular events or transient ischemia and a factor predictive of recurrent cerebrovascular events. Serum fibrinogen level is correlated with the progression of carotid lesions. Finally, fibrinogen is an independent predictive factor of the severity of atherosclerosis of the thoracic aorta, lower limb arteriopathy, and more generally silent atherosclerotic plaques. PERSPECTIVES: A large-scale prospective study is needed to determine whether drug-induced reduction in serum fibrinogen can reduce the rate of cardiovascular events.

Adult↗
PubMed2000

[Effect of methyclothiazide on the entry of calcium into vascular smooth muscle cells].

The possible involvement of calcium and potassium channels in mediating the vascular actions of methyclothiazide (MCTZ), a thiazide diuretic, was investigated in isolated aortic rings from 12 week-old hypertensive rats. MCTZ (10(-4) M) inhibits the contractile response induced by addition of Ca2+ to a depolarizing solution, the maximal contracture is reduced by 87.16 +/- 6.4%. Furthermore this inhibitory effect was unaffected by charybdotoxine a selective blocker of calcium-activated K+ channels (Kca). This suggesting that MCTZ inhibits voltage-gated Ca2+ channels and blunts the Ca2+ entry into vascular smooth muscle cells. This inhibition was partially attenuated by either mechanical removal of the endothelium or N omega-nitro-L-arginine (NOLA) treatment, suggesting that MCTZ effects are also mediated by an endothelium-dependent mechanism involving endothelium-dependent relaxing factor (EDRF)/nitric oxide (NO) release. Taken together, these observations could point to a role of voltage-gated Ca2+ channels and endothelial release of EDRF/NO in the antihypertensive action of MCTZ.

Animals↗
PubMedDate not supplied

Direct vascular actions of methyclothiazide and indapamide in aorta of spontaneously hypertensive rats.

In vitro experiments were designed to assess the inhibitory effect of the thiazide diuretics methyclothiazide (MCTZ), the hydrochlorothiazide (HCTZ), and the thiazide-related diuretic indapamide (IND) on contractile responses to norepinephrine (NE) and arginine vasopressin (AVP) of aortic rings from spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). Changes in the tension of aortic ring preparations were measured isometrically. MCTZ (10(-4) M) induced endothelium-dependent inhibition of the vasoconstrictor responses to NE and AVP only in aortas from SHR, and the maximal vasoconstrictive effect of NE and AVP was decreased by 59 +/- 11% and 32.3 +/- 13%, respectively. Indapamide (10(-4) M) also induced endothelium-dependent inhibition of the contractile response to AVP in aortic rings from SHR, and the maximal vasoconstrictive effect of AVP was decreased by 33 +/- 5%. In contrast, HCTZ did not inhibit the contractile response to either NE or AVP, even at the highest concentration. This study provides evidence that methyclothiazide and indapamide inhibit the contractile response induced by norepinephrine and/or arginine vasopressin on SHR aortic preparations via an endothelium-dependent mechanism.

Animals↗