Drugs online research references
Nippon Ronen Igakkai Zasshi. 1994 Apr;31(4):285-92.
[Effect of nifedipine and enalapril on cardiac autonomic activity in elderly hypertensive patients]
[Article in Japanese]
Okabayashi J, Matsubayashi K, Sato T, Ozawa T.
Department of Medicine and Geriatrics, Kochi Medical School.
To clarify the effect of the calcium antagonist Nifedipine and the ACE inhibitor Enalapril on cardiac autonomic activity, power spectral analysis of heart rate variability (PSA) was conducted in 39 elderly patients with essential hypertension (mean age: 63: +/- 11 years) before and after treatment. Twenty patients were treated with 10-20 mg of Nifedipine (N group) and 19 with 5 mg of Enalapril (E group) for 3 months. beta-blocker (Atenolol 12.5 mg) was added to Nifedipine in 12 patients of the N group for 1 month, and the modified effect of Atenolol on cardiac autonomic activity was also evaluated. Blood pressures were significantly reduced in both N and E groups after the treatment. The low frequency component (LF) in PSA, which was considered to be a quantitative marker of cardiac sympathetic activity, increased significantly and the high frequency component (HF), which was a marker of cardiac parasympathetic activity, significantly decreased with increase of PNA levels in N group after the treatment. However, the LF decreased significantly after addition of Atenolol. On the other hand, there was little significant change in LF and PNA in E group. These results suggest that Nifedipine increased cardiac sympathetic activity and that Enalapril had little influence on the cardiac sympathetic tone, while both antihypertensive agents significantly reduced blood pressure itself.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8041023&dopt=Abstract
J Physiol. 1993 Nov;471:583-97.
The modulatory effects of endothelin-1, carbachol and isoprenaline upon Na(+)-H+ exchange in dog cardiac Purkinje fibres.
Wu ML, Tseng YZ.
Department of Physiology, Medical College, National Taiwan University, Taipei, R.O.C.
1. The modulatory effects of carbachol, endothelin-1 and isoprenaline upon Na(+)-H+ exchange were examined in dog cardiac Purkinje fibres. Intracellular pH (pHi) and intracellular sodium activity (aiNa) were recorded using pH and Na(+)-selective microelectrodes. Acid extrusion via Na(+)-H+ exchange was estimated from the pHi recovery rate (multiplied by intrinsic buffering power (beta i) and adding mean background acid load) in response to an internal acid load induced by the removal of 20 mM NH4Cl. All experiments in this work were performed in Hepes-buffered solutions at 37 degrees C. 2. beta i was estimated at various values of pHi in the range of 7.4-6.4 and was calculated from the fall of pHi induced by the addition and removal of NH4Cl. Experiments were performed when Na(+)-H+ exchange was blocked. The values of beta i in this tissue were only slightly dependent on pHi in the range of 7.4-6.4 with an empirical relationship: beta i = -4.69 pHi + 64.59. 3. Endothelin-1 (10(-8) M) alkalinized the resting pHi by approximately 0.1 pH unit and accelerated acid extrusion, by approximately 96%, at pHi approximately 6.9. A reduction of background acid loading within the cell cannot account for the augmentation of pHi recovery, since the rate of acid extrusion was not changed either at resting pHi or at internal acidification in Na(+)-free solution (a measure of background loading) by the addition of endothelin-1. The protein kinase C inhibitors staurosporin (10(-6) M) and 1-(5-isoquinolinylsulphonyl)-2-methyl-piperazine (H-7, 50 microM) could not block the effect of endothelin-1 on the antiporter. 4. At pHi approximately 6.8, carbachol (7.5 x 10(-4) M) accelerated pHi recovery by approximately 68% and alkalinized the resting pHi by approximately 0.1 pH unit. This stimulatory effect of carbachol was completely blocked by pretreatment with atropine (10(-4) M) and staurosporine 10(-6) M. The background acid load was not reduced by adding carbachol, since the acid extrusion during pHi recovery or at the resting state was not affected by the addition of carbachol to a sodium-free solution. 5. Isoprenaline (10(-6) M) slowed pHi recovery by approximately 45% measured at pHi 6.9 with no change in resting pHi. A rise in background acid loading could not account for the reduction of acid extrusion. Pretreated with atenolol (10(-6) M), a beta 1-selective antagonist, completely blocked the effect of isoprenaline.(ABSTRACT TRUNCATED AT 400 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8120823&dopt=Abstract
J Hypertens. 1984 Feb;2(1):43-8.
Beta-adrenergic blockade alone does not decrease renal perfusion in black hypertensives.
Brater DC, Anderson S, Kaplan NM, Ram CV.
We assessed the effects on renal haemodynamics in 18 black patients with essential hypertension of acute and chronic beta-adrenergic blockade with three agents having different properties: atenolol, nadolol or propranolol. Six patients received each drug. In our patients the antihypertensive response to beta-blockers was minimal or nonexistent. This permitted us to analyse the effects on renal haemodynamics of 'pure' beta-blockade, as opposed to the combined effects of beta-blockade and decreased systemic perfusion pressure. In this setting, neither acute nor chronic administration (two months) of each of these agents decreased renal perfusion. We conclude, therefore, that beta-blockade per se has no deleterious effect on renal function and previous observations are most probably accounted for by the blood pressure lowering effect of these drugs, either alone or coupled with beta-blockade of the renal vasculature allowing unopposed alpha-sympathetically mediated vasoconstriction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6152277&dopt=Abstract
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