Are sodium-dependent V1 receptors and sympathetic nerve activations involved in regulation of blood pressure in borderline-hypertensive Hiroshima rats?
Sympathetic nerve activity (SNA) was estimated by the magnitude of depressor response after ganglionic blockade with hexamethonium bromide (C6; 25 mg/kg weight). The depressor effects of C6 were significantly less in borderline-hypertensive Hiroshima rats (BHR) than in deoxycorticosterone acetate (DOCA)-salt hypertensive rats (DOCA rats) or in spontaneously hypertensive rats (SHR), but they were not different in BHR and normotensive control Wistar rats (NCR). After sympatho-inhibition, the depressor effects of a selective vasopressin V1 receptor antagonist (V1A; 10 microg/kg: [d(CH2)5(1), O-Me-Tyr2, Arg8]-vasopressin) were significantly greater in BHR than in DOCA rats, SHR or NCR. In a previous study, we reported that the depressor effects of C6 were significantly less in BHR than in SHR, but after sympatho-inhibition, the depressor effects of V1A were significantly greater in BHR than in SHR (Hypertens Res 2002; 25: 241-248). After high-salt diet loading in the present study (8% salt-containing diet for 10 weeks), the magnitudes of increase in mean arterial pressure in BHR and NCR were almost the same. There was almost no difference in the depressor effects of V1A after sympatho-inhibition between BHR with high-salt intake and BHR without high-salt intake. The depressor effects of an angiotensin-converting enzyme inhibitor, captopril (1 mg/kg), were almost the same between BHR and NCR both before and after sympatho-inhibition. However, these effects were completely inhibited after the high-salt diet. The results show that SNA was within the normal range in BHR and that no further accelerated responsiveness of endogenous vasopressin was observed in BHR after high-salt intake.
Teranishi
Yasuhiro
Y
Department of Physiology, Faculty of Medicine, Hiroshima University, Hiroshima, Japan. ytera@hiroshima-u.ac.jp
Kumazaki
Tsutomu
T
Miho
Narimasa
N
Sugino
Hiroshi
H
Tsuru
Hiromichi
H
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002216:Captopril / Q000494:pharmacology; D003243:Consciousness; D005730:Ganglionic Blockers / Q000494:pharmacology; D006339:Heart Rate / Q000502:physiology; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology*; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR; D011922:Rats, Mutant Strains; D017208:Rats, Wistar; D017483:Receptors, Vasopressin / Q000378:metabolism*; D012084:Renin-Angiotensin System / Q000502:physiology; D012146:Rest / Q000502:physiology; D012964:Sodium / Q000378:metabolism; D017673:Sodium Chloride, Dietary / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*
D000806:Angiotensin-Converting Enzyme Inhibitors; D065092:Antidiuretic Hormone Receptor Antagonists; D005730:Ganglionic Blockers; D017483:Receptors, Vasopressin; D017673:Sodium Chloride, Dietary; D002216:Captopril; D012964:Sodium