Tojo A, Kimura K, Matsuoka H, Sugimoto T
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
J Cardiovasc Pharmacol. 1992 Dec;20(6):895-9. doi: 10.1097/00005344-199212000-00008.
We wished to clarify the effects of a newly developed calcium antagonist, manidipine hydrochloride (HCl), on renal microcirculation in hypertensive rats by using the micropuncture technique. Oral administration of manidipine HCl for 2 months reduced systemic blood pressure (BP), did not change the single-nephron glomerular filtration rate (SNGFR), but increased the SNG plasma flow (SNGPF). Moreover, the glomerular transcapillary hydraulic pressure difference (delta P), which is assumed to be the parameter most related to development of glomerulosclerosis, was significantly reduced. Both afferent and efferent arteriolar resistance (RA and RE) were reduced. Intravenous (i.v.) infusion of manidipine HCl (20 micrograms/kg) decreased systemic BP but did not change SNGFR, SNGPF, or delta P. Both RA and RE were also significantly decreased. These results indicate that chronic administration of manidipine HCl increases renal blood flow (RBF) by dilating the afferent arterioles and improves glomerular hypertension by dilating the efferent arterioles. Thus, manidipine HCl might be a beneficial antihypertensive agent for patients with renal diseases. Because acute i.v. infusion of manidipine HCl did not change delta P, apparently time must elapse before glomerular hypertension is corrected.
