title: Renal depressor mechanisms of physical training in patients with essential hypertension.
abstract: To clarify characteristics of the patients in whom exercise training lowers blood pressure and to elucidate the mechanisms by which exercise training lowers blood pressure, we evaluated 24-h blood pressure, glomerular filtration rate (GFR), renal blood flow (RBF), filtration fraction (FF), plasma renin activity (PRA), plasma aldosterone concentration (PAC), plasma norepinephrine concentration (PNE), and incremental area of insulin/glucose (sigmaI/sigmaG) during 75 g oral glucose tolerance test, and assessed arterial baroreceptor function (BSI) before and after a 3-week exercise training program (four 6-min sessions daily at 75% VO2 max). Patients were classified as responders (n = 15) if they showed statistically significant reduction in the multiple comparison of 24-h mean arterial pressure (MAP), or as nonresponders (n = 15) if they did not. Although there were no significant differences between responders and nonresponders in age, weight, MAP, GFR, RBF, RPF, FF, PNE, sigmaI/sigmaG, or BSI before exercise, renal vascular resistance (RVR; P < .05), PRA (P < .05), and PAC (P < .05) were significantly higher in responders than in nonresponders. The fractional excretion of sodium (FENa) (P < .05) were significantly lower in responders than in nonresponders. After exercise training, FF (P < .01), RVR (P < .05), PNE (P < .05) PRA (P < .01), and sigmaI/sigmaG (P < .05) decreased significantly only in responders. The decrease in MAP significantly correlated with the reductions in FF (r = 0.46, P < .05), PNE (r = 0.52, P < .01) and RVR (r = 0.40, P < .05). Thus, in patients who have higher RVR and PRA, exercise training lowered blood pressure in parallel to a reduction in RVR associated with decreases in sympathetic tone and improvement of insulin resistance. Our results suggest that exercise-induced changes in renal hemodynamics may contribute to the reduction in blood pressure in these patients.
authors.affiliation: Department of Internal Medicine III, Kurume University School of Medicine, Fukuoka, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kohno
authors.forename: H
authors.initials: H
authors.lastname: Matsuoka
authors.forename: K
authors.initials: K
authors.lastname: Takenaka
authors.forename: Y
authors.initials: Y
authors.lastname: Miyake
authors.forename: G
authors.initials: G
authors.lastname: Nomura
authors.forename: T
authors.initials: T
authors.lastname: Imaizumi
mesh_terms: D000328:Adult; D017704:Baroreflex / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D018660:Blood Pressure Monitoring, Ambulatory; D015444:Exercise / Q000502:physiology*; D005260:Female; D005951:Glucose Tolerance Test; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology*; D007677:Kidney Function Tests; D008297:Male; D018377:Neurotransmitter Agents / Q000097:blood; D010101:Oxygen Consumption / Q000187:drug effects; D010806:Physical Education and Training; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology; D012964:Sodium / Q000652:urine
chemical_list: D018377:Neurotransmitter Agents; D012964:Sodium