Drugs online research references
Acta Med Scand. 1983;213(5):381-5.
Complaints of cold extremities among patients on antihypertensive treatment.
Feleke E, Lyngstam O, Rastam L, Ryden L.
A total of 758 consecutive patients attending three hypertension clinics answered a questionnaire designed to assess the prevalence and severity of complaints of cold extremities among patients on various antihypertensive drugs. Forty-four per cent claimed to have had complaints of cold extremities and about 50% of these had had symptoms already prior to antihypertensive treatment. Among the newly symptomatic patients the prevalence of symptoms was 18% of those on diuretics and 40% of those on beta-blockers (p less than 0.01). No significant association was found between the prevalence of symptoms and age, sex, use of vibrating tools, smoking or history of various conditions associated with atherosclerosis. No significant difference was found in the prevalence of symptoms among patients on propranolol, alprenolol, pindolol, atenolol and metoprolol. It is concluded that cold hands and feet are common among hypertensive patients and may be aggravated by treatment with not only beta-blockers but also diuretics.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6136158&dopt=Abstract
J Auton Pharmacol. 1989 Apr;9(2):103-11.
Enhanced presynaptic facilitation of vascular adrenergic neurotransmission in spontaneously hypertensive rats.
Draper AJ, Meghji S, Redfern PH.
Pharmacology Group, School of Pharmacy and Pharmacology, University of Bath, Claverton Down, UK.
1. The interaction between the vascular renin-angiotensin system and presynaptic beta-adrenoreceptors was examined in male and female normotensive and spontaneously hypertensive rats, using the in vitro perfused mesentery preparation. 2. Enhancement of the pressor response to periarterial nerve stimulation by isoprenaline was shown to be significantly greater in preparations from male and female spontaneously hypertensive rats compared to corresponding preparations from normotensive Wistar rats. 3. In preparations from normotensive and hypertensive animals, the potentiating effect of isoprenaline was prevented by pretreatment with propranolol or ICI 118 551, but not atenolol, implicating a beta 2-adrenoreceptor. 4. Angiotensin II enhanced the responses to peripheral nerve stimulation in preparation from normotensive and hypertensive animals. Enhancement was significantly greater in preparations from hypertensive animals. 5. The potentiation caused by isoprenaline was blocked by the angiotensin II receptor antagonist [Sar1-Ile8] angiotensin II, and by captopril. The potentiation following angiotensin II was unaffected by ICI 118 551. 6. These results suggest that stimulation of presynaptic beta 2-adrenoreceptors activates a localized angiotensin II system. No significant differences in this facilitatory system were observed between male and female animals, but the potentiation caused by activation of this system was considerably greater in the spontaneously hypertensive rats.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2565899&dopt=Abstract
J Pharmacol Exp Ther. 1987 Dec;243(3):1107-12.
Beta adrenoceptor facilitation of norepinephrine release is not dependent on local angiotensin II formation in the rat isolated kidney.
Rump LC, Majewski H.
Department of Pharmacology, University of Melbourne, Victoria, Australia.
The aim of the study was to investigate beta adrenoceptor modulation of norepinephrine release from sympathetic nerves in rat isolated kidney. After preincubation with [3H]norepinephrine, the renal nerves were stimulated at 1 Hz. The stimulation induced (S-I) outflow of radioactivity was taken as an index of norepinephrine release. Isoproterenol (0.1 microM) enhanced the S-I outflow of radioactivity. This effect was abolished by the beta-2 adrenoceptor blocking drug ICI 118551 (0.1 microM) but unaltered by the beta-1 adrenoceptor blocking drug atenolol (0.3 microM). In the presence of a high concentration of the angiotensin converting enzyme inhibitor captopril (5 microM), isoproterenol failed to enhance the S-I outflow of radioactivity. However, a lower concentration of captopril (0.1 microM), which totally abolished the facilitatory effect of angiotensin I (0.1 microM) on the S-I outflow of radioactivity, failed to alter the facilitatory effect of isoproterenol. Angiotensin II (0.03 microM) enhanced markedly the S-I outflow of radioactivity and in the presence of the angiotensin II receptor blocking drug saralasin (0.1 microM) this facilitatory effect was reduced markedly. Saralasin did not alter the facilitatory effect of isoproterenol. These results suggest that stimulation of prejunctional beta-2 adrenoceptors on renal sympathetic nerve endings enhances norepinephrine release. This effect is independent of local angiotensin II production and does not involve activation of prejunctional angiotensin II receptors within the rat kidney. However, the inhibitory effect of a high concentration of captopril (5.0 microM) on beta-2 adrenoceptor-mediated facilitation of norepinephrine release remains to be clarified.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2826755&dopt=Abstract
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