Effects of Substance P, Angiotensin II, Oxotremorine and Prostaglandin D2 on Thyrotropin Secretion in Rats

1984 ◽  
Vol 19 (3) ◽  
pp. 176-184 ◽  
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori
Keyword(s):  
Angiotensin Ii ◽  
Substance P

Angiotensin II- and substance P-like immunoreactivity in human follicular fluid: correlation of the peptide content with follicle size

1987 ◽  
Vol 116 (3_Suppl) ◽  
pp. S117-S118
Author(s):  
H. JARRY ◽  
B. MEYER ◽  
G. HOLZAPFEL ◽  
B. HINNEY ◽  
D. TEMME ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Substance P ◽  
Follicular Fluid ◽  
Human Follicular Fluid ◽  
Follicle Size

scholarly journals Hemolysate Inhibits Cerebral Artery Relaxation

1988 ◽  
Vol 8 (1) ◽  
pp. 46-53 ◽  
Author(s):  
Noboru Toda
Keyword(s):  
Methylene Blue ◽  
Angiotensin Ii ◽  
Substance P ◽  
Cerebral Arteries ◽  
Vascular Wall ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Middle Cerebral Arteries ◽  
Relaxant Response ◽  
Stimulation Of

In helical strips of dog middle cerebral arteries partially contracted with prostaglandin (PG) F2α, relaxations induced by angiotensin-II, possibly mediated by PGI2, and those induced by PGH2 were reversed to a contraction or markedly reduced by treatment with hemolysate, which, however, attenuated the PGI2-induced relaxation only slightly. The relaxant response of human middle cerebral arterial strips to PGH2 was also suppressed by hemolysate. Dog and monkey middle cerebral arteries responded to transmural electrical stimulation and nicotine with transient relaxations, which were quite susceptible to tetrodotoxin and hexamethonium, respectively; the relaxations were abolished almost completely by hemolysate and methylene blue. On the other hand, the relaxant response of dog cerebral arteries to a low concentration of K+ was not influenced by hemolysate or by methylene blue, but was reversed to a contraction by treatment with ouabain. Relaxations induced by substance-P and nitroglycerin were markedly inhibited by hemolysate; removal of endothelium abolished the relaxation by substance-P, but did not influence the nitroglycerin-induced relaxation. Hemolysate may interfere with the biosynthesis of PGI2 in the vascular wall, thereby reversing the relaxation induced by angiotensin-II and PGH2 to a contraction. Relaxations induced by electrical and chemical stimulation of vasodilator nerves innervating cerebral arteries appear to be elicited by a mechanism dependent on cellular cyclic guanosine monophosphate (GMP), like that underlying the substance-P-induced and nitroglycerin-induced relaxation. These actions of hemolysate may be involved in the genesis of cerebral vasospasm after subarachnoid hemorrhage.

Effects of sodium depletion on the response of rat adrenal zona glomerulosa cells to stimulation by neuropeptides: actions of vasoactive intestinal peptide, enkephalin, substance P, neuropeptide Y and corticotrophin-releasing hormone

1995 ◽  
Vol 146 (2) ◽  
pp. 209-214 ◽  
Author(s):  
J P Hinson ◽  
S Kapas
Keyword(s):  
Angiotensin Ii ◽  
Substance P ◽  
Neuropeptide Y ◽  
Vasoactive Intestinal Peptide ◽  
Zona Glomerulosa ◽  
Angiotensin Ii Receptors ◽  
Sodium Depletion ◽  
Aldosterone Secretion ◽  
Glomerulosa Cells ◽  
Zona Glomerulosa Cells

Abstract There are several neuropeptides, present in nerves supplying the rat adrenal zona glomerulosa, which have been shown to stimulate aldosterone secretion in the intact perfused rat adrenal preparation. The purpose of the present study was twofold: first, to determine whether these peptides acted directly on adrenocortical cells by examining their effects on collagenase-dispersed rat zona glomerulosa cells, and second, to investigate the likely physiological significance of these actions, by determining whether the responses of zona glomerulosa cells to neuropeptides were changed by prior sodium depletion. Of the peptides tested, neuropeptide Y (NPY) and substance P had only a minor effect on aldosterone secretion, which was not substantially affected by sodium depletion. Corticotrophin-releasing hormone (CRH) had a significant stimulatory effect on aldosterone secretion, but neither the threshold concentration for significant stimulation nor the maximal response to stimulation were altered by prior sodium depletion. Vasoactive intestinal peptide (VIP), on the other hand, had little effect on aldosterone secretion by cells from normal animals, but was a potent stimulus to aldosterone secretion in cells obtained from sodium-depleted animals. The response to the Met-enkephalin analogue, [d-Ala2-Met2]-enkephalinamide (DALA), was also significantly enhanced by prior sodium depletion. Experiments using the angiotensin II receptor blocker, saralasin, were carried out to determine whether the enhanced actions of DALA and VIP seen in sodium depletion may be a result of activation of angiotensin II receptors, known to be increased in sodium depletion. Saralasin did not affect the response to either peptide. These data suggest that all the peptides tested may be able to stimulate aldosterone secretion. However, the data obtained with substance P, NPY and CRH do not support a major role for these peptides in the regulation of aldosterone secretion either under control conditions, or in sodium depletion. The finding that the responses to VIP and DALA were altered by sodium depletion suggests that the actions of VIP and opioid peptides may have physiological significance in the regulation of aldosterone secretion in response to sodium depletion. Furthermore, the observation that saralasin does not inhibit the responses to these peptides strongly suggests that they are not acting through angiotensin II receptors, and may indicate altered VIP- and opioid-receptor regulation in sodium depletion. Journal of Endocrinology (1995) 146, 209–214

Acute depressor actions of angiotensin II in the nucleus of the solitary tract are mediated by substance P

1997 ◽  
Vol 273 (1) ◽  
pp. R28-R34 ◽  
Author(s):  
D. I. Diz ◽  
D. L. Fantz ◽  
I. F. Benter ◽  
S. M. Bosch
Keyword(s):  
Angiotensin Ii ◽  
Substance P ◽  
Cardiovascular Effects ◽  
Solitary Tract ◽  
Sprague Dawley ◽  
Induced Hypotension ◽  
Sprague Dawley Rats ◽  
Substance P Antagonist ◽  
Before And After

Angiotensin II stimulates release of substance P from medulla oblongata slices, and low doses of substance P or angiotensin II injected into the nucleus of the solitary tract (NTS) decrease heart rate and mean arterial pressure. In this study, angiotensin II (250 fmol in 30 nl) was injected into the NTS of halothane-anesthetized male Sprague-Dawley rats before and after NTS injections of the substance P antagonist [Leu11, psi CH2NH-(10-11)]substance P (600 fmol in 60 nl). The substance P antagonist blocked the angiotensin II-induced hypotension and bradycardia (-16 +/- 3 mmHg and -24 +/- 7 beats/min before versus -0.3 +/- 1 mmHg and -2 +/- 3 beats/min after; P < 0.05). The depressor and bradycardic effects of glutamate were not altered by the substance P antagonist. In vitro receptor autoradiography showed that the substance P antagonist (10 or 100 microM) did not compete for 125I-labeled angiotensin II binding in the dorsal medulla, suggesting that the substance P antagonist does not interact directly with angiotensin II receptors. We conclude that the cardiovascular effects of angiotensin II in the NTS are mediated at least in part by substance P.

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