Effects of substance P on norepinephrine release from vascular adrenergic neurons in spontaneously hypertensive rats

• Published in: American journal of hypertension Vol. 4; no. 4 Pt 1; p. 327
• Main Authors: Tsuda, K, Masuyama, Y
• Format: Journal Article
• Language: English
• Published: United States 01.04.1991
• Subjects: Adrenergic Fibers - drug effects; Adrenergic Fibers - metabolism; Animals; Blood Pressure - drug effects; Electric Stimulation; Hypertension - physiopathology; In Vitro Techniques; Male; Mesenteric Arteries - drug effects; Mesenteric Arteries - innervation; Mesenteric Arteries - metabolism; Norepinephrine - metabolism; Norepinephrine - pharmacology; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Substance P - pharmacology
• ISSN: 0895-7061
• DOI: 10.1093/ajh/4.4.327

This study was performed to investigate the role of substance P in the vascular adrenergic transmission in hypertension. In perfused mesenteric vasculatures prepared from spontaneously hypertensive rats (SHR, 7 to 10 weeks old) and age-matched Wistar-Kyoto rats (WKY), we have examined the effects of substance P on vascular responsiveness as well as on norepinephrine release from the vascular adrenergic neurons. In preliminary studies with normotensive Wistar rats, pressor responses and endogenous norepinephrine release during electrical nerve stimulation were inhibited by substance P in a dose-dependent manner. However, vasoconstrictor responses to exogenous norepinephrine were not affected by the peptide. In SHR, the stimulation-evoked pressor responses and norepinephrine release were enhanced compared with WKY. Alternatively, the suppression of these responses by substance P was significantly less in SHR than in WKY. These results demonstrate that substance P could have a modulatory effect on noradrenergic activity and cause a decrease in stimulation-evoked norepinephrine release from the vascular adrenergic neurons. The attenuated reduction of pressor responses and norepinephrine release by substance P in SHR might suggest insufficient regulation of vascular adrenergic transmission by the peptide in hypertension.