Drugs online research references
Life Sci. 1994;54(24):PL451-6.
Role of alpha 1-adrenoceptor subtypes which mediate positive chronotropy in neonatal rat cardiac myocytes.
Kimura H, Kawana S, Kanaya N, Sakano S, Miyamoto A, Ohshika H.
Department of Pharmacology, School of Medicine, Sapporo Medical University, Japan.
We investigated the involvement of alpha 1-adrenoceptor subtypes in the positive chronotropic response to norepinephrine (NE) in neonatal rat cardiac myocytes at day 3 of culture. The cardiac myocytes at day 3 of culture exhibited a dose-dependent positive chronotropic response to NE in the presence of propranolol, a beta-adrenoceptor antagonist. The positive chronotropic responses to NE were completely antagonized by the alpha 1-adrenoceptor antagonist prazosin. The NE-induced positive chronotropic response was inhibited 68% by the alpha 1B-adrenoceptor antagonist, chloroethylclonidine (CEC), but partially (41%) so by the alpha 1A-adrenoceptor antagonist, WB4101. In the membrane fraction derived from cardiac myocytes at day 3 of culture, pretreatment with CEC decreased the Bmax of the alpha 1-adrenoceptor to 22% of the control value. The NE-induced positive chronotropic response was inhibited 62 and 77% by the voltage-gated Ca2+ channel blocker such as nifedipine and verapamil, respectively. These findings indicate (1) that cultured neonatal rat cardiac myocytes possess both alpha 1-adrenoceptor subtypes, i.e., alpha 1A and alpha 1B, (2) that the predominant alpha 1-adrenoceptor subtypes mediating NE-induced positive chronotropy in neonatal rat cardiac myocytes at day 3 of culture are alpha 1B-subtypes, and (3) that NE-induced positive chronotropy may be caused via voltage-gated Ca2+ channel activation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8196500&dopt=Abstract
fac.howard.edu
We studied the role of sarcolemmal alpha- and beta-adrenoceptors activation in the effects of cocaine on the positive force staircase in isolated guinea pig atria. The preparations were superfused with Tyrode's solution at 31 degrees C while attached to a force transducer to measure peak tension developed (PTD), maximum velocity of development of tension (Vmax T) and time to peak tension (TPT). The positive force staircase was not affected by propranolol or phentolamine, but it was abolished by nifedipine. Cocaine 1 mg/l (2.9 microM) enhanced PTD and Vmax T, while TPT remained unchanged. On the other hand, cocaine did not modify the increase in PTD induced by the increase in frequency of stimulation, but significantly reduced the magnitude of the increase in Vmax T. The cocaine-induced attenuation of the increase in Vmax T in response to changes in the frequency of stimulation was abolished by both propranolol and phentolamine. It is concluded that the effect of cocaine on the force-frequency relationship required background activation of alpha- and beta-adrenergic receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9734706&dopt=Abstract
Res Commun Chem Pathol Pharmacol. 1994 Feb;83(2):125-44.
Effects of dietary vitamin D deficiency on the cardiovascular system.
De Novellis V, Loffreda A, Vitagliano S, Stella L, Lampa E, Filippelli W, Vacca C, Guarino V, Rossi F.
Institute of Pharmacology and Toxicology, II University of Naples, Italy.
Experiments were performed on normotensive rats exposed to vitamin D deficient and control diets from the 22nd to the 180th day of age. In 60-120- and 180-day-old rats. The following parameters were evaluated: a) The vasomotor responses elicited by receptor agonists in the absence and in the presence of the respective antagonists [L-norepinephrine (NE) before and 5 min after prazosin; L-isoprenaline (I) before and 5 min after DL-propranolol; L-dopamine (DA) before and 5 min after L-sulpiride or SCH 23390 or chlorpromazine; acetylcholine (Ach) before and 5 min after atropine; histamine (H) before and after chlorpheniramine; 5-hydroxytryptamine (5-HT) before and 5 min after methysergide or ketanserin]; by carotid-sinus baroreceptor stimulation (CO) before and 5 min after hexamethonium, and by electrical stimulation of the vagus peripheral head (V) before and after atropine; b) Reflex tachycardia elicited by bilateral carotid occlusion (CO) (for 40 sec) and by sodium nitroprusside; c) Catecholamine (norepinephrine, epinephrine) and arginine-vasopressin plasma levels; d) Cholesterol, triglyceride and electrolyte (Na+, K+, Cl-, Ca2+) serum levels. Our results showed that vitamin D deficient diets induced a decrease in pressor responses to NE and CO, and an increase in hypotensive responses to I, DA, Ach, H, 5-HT and V. Changes of arterial blood pressure, heart rate, catecholamine and arginine-vasopressin plasma levels were not observed. Cholesterol, triglyceride and electrolyte (Na+, K+, Cl-) serum levels were not modified, while Ca2+ serum levels decreased. In conclusion, our data suggest that vitamin D depletion can induce changes of pressor and depressor vasomotor responses and suppose a direct role for vitamin D in regulating vasomotor reactivity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8202626&dopt=Abstract
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