Search

The sympathetic tone of the splanchnic nerve was quantified in renal and deoxycorticosterone (DOC) hypertensive rats under pentobarbital anesthesia by measuring equivalent stimulation frequency (ESF). ESF is the frequency of stimulus to the peripheral cut end of the nerve required to restore the preseverance level of arterial pressure. It is assumed to represent the average discharge rate of the nerve before severance. ESF was markedly increased in DOC hypertension 2 weeks after initiation of the DOC-salt treatment. It was relatively decreased after 10 weeks, but was still higher than in the controls. In renal hypertension (clipping of the left renal artery), ESF was decreased considerably 2 weeks and slightly 10 weeks after clipping. When the contralateral kidney had been removed simultaneously with clipping (clip plus uninephrectomy, ESF was not significantly changed. It is suggested that the sympathetic nervous system participates greatly in the pathogenesis of DOC hypertension but not of renal hypertension.

Utilizing the microsurgical method of transplantation in the rat, the role of the kidney in an experimental renal hypertension due to segmental renal infarction was studied. When the infarcted kidney was transplanted into the bilaterally nephrectomized recipient, hypertension developed so long as the donor kidney was transplanted within 2 weeks after infarction. With transplantation of the normal kidney into the hypertensive rat 8 weeks after infarction, BP remained high unless the infarcted kidney was removed. PRA after transplantation, or KRA of the transplanted kidneys were not correlated to the blood pressure levels. It was suggested that the infarcted kidney has the pressor mechanism, lasting for 2 weeks or more after infarction. The infarcted kidney also has the maintenance mechanism, establishing 8 weeks after infarction.

The F1 hybrids (F1) of spontaneously hypertensive rats (SHR) and Wistar rats (W), whose kidneys were transplanted from SHR at the age of 10 weeks and 20 weeks, showed significant elevation of blood pressure (BP) for 11 weeks after the transplantation. In F1 with W or F1 kidneys BP was decreased near to the normal level. F1 whose kidneys were transplanted from SHR or W showed low renin activity both in plasma and the kidney. It is suggested that BP of SHR is probably determined by the renal pro-hypertensive factor(s) other than renin influencing on sympathetic nerves through central nervous systems.

A prospective survey on the comparative studies of the renin-angiotensin system (RAS) was made at the final session of the Japan-U.S. Cooperative Seminar, held on November 14--19, 1977, at Jichi Medical School, Tochigi-ken, Japan. Strategies and tactics of the research have been clarified. In morphological studies, the strategy is to clarify structure of the juxtaglomerular apparatus in representative species of vetebrate classes. In chemical studies, each component of the RAS must be established in each vertebrate class. Since we now know the existence of severel new angiotensins in vertebrates, their amino-acid sequences must be determined. They must be synthesized in sufficient purity. It is necessary to establish the international purity and assay criteria for synthetic angiotensins. In comparative studies on physiological aspects, the strategy is to establish the physiological roles of the RAS in vertebrate classes. Controls of blood pressure, of aldostrone secretion, of glomerular filtration rate and tubular transport, and of drinking and intestinal absorpiton are the candidates. Physiological roles of extrarenal renin as well as renal one are interesting. A renin-like substance in the corpuscles of Stannius in the teleosts has been identified preliminarily as hypocalcin. Many frontiers exist in these fields, and one can expect fruitful contributions to research of the cardiovascular disease in humans through comparative studies of the RAS.

As a discrepancy exists between two reports from our laboratory on plasma renin activity (PRA) in spontaneously hypertensive rats (SHR), we undertook to examine the reasons for this discrepancy. PRA in SHR at 15 weeks of age was determined by two different methods, utilizing the procedures of Boucher et al or of Haber et al. For normotensive controls, Donryu (DON) and Wistar-Kyoto (WKY) rats were used. By Boucher's method, PRA in SHR was significantly lower than in DON, but did not differ from WKY. By Haber's method, PRA in SHR did not significantly differ from DON or WKY. However, the value in DON was significantly higher than in WKY. The present study basically confirmed our previous results, concluding that PRA in SHR at 15 weeks of age is within the normal range. A previous suggestion that PRA in SHR is suppressed as a result of blood pressure elevation must be revised, because it was derived from results considering only the DON strain as the control.