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Renal hemodynamic changes during smoking: effects of adrenoreceptor blockade
Author(s) -
Urs Benck,
Clorius Jh,
I. Zuna,
Eberhard Ritz
Publication year - 1999
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1999.00566.x
Subject(s) - atenolol , medicine , prazosin , hemodynamics , renal function , blood pressure , plasma renin activity , renal blood flow , placebo , endocrinology , filtration fraction , kidney , renin–angiotensin system , antagonist , receptor , alternative medicine , pathology
Background Cigarette smoking accelerates progression of renal failure in diabetic and nondiabetic renal disease. Renal hemodynamics during smoking are characterised by a reversible decrease in glomerular filtration rate (GFR) and filtration fraction (FF) accompanied by increased renovascular resistance (RVR), systemic blood pressure, heart rate and plasma catecholamine concentrations. Materials and methods To further assess the role of sympathetic overactivity we compared the effects of different pharmacological interventions on smoking‐induced changes of renal hemodynamics in occasional smokers. In a first series, placebo pretreatment plus smoking was compared to Prazosin pretreatment (3 mg) plus smoking. In a second study, placebo pretreatment plus smoking was compared to Atenolol pretreatment (50 mg) plus smoking. Results Basal blood pressure was significantly lower with Prazosin and Atenolol. On placebo, GFR and FF decreased significantly during smoking and RVR increased. With Prazosin pretreatment compared to placebo pretreatment no statistically significant differences for the changes of GFR, FF, RPF and RVR were seen. In contrast, with Atenolol pretreatment compared to placebo pretreatment, the smoking‐induced changes in active renin, GFR and RVR were significantly smaller. Conclusion It is suggested that the acute renal hemodynamic effects of smoking are mediated, at least in part, via increased sympathetic activity operating mainly through beta‐1 adrenergic mechanisms.