|1.||Hong, Jason Kyung-soo: 1 article (08/2009)|
|2.||Figueroa, Jorge P: 1 article (08/2009)|
|3.||Diz, Debra I: 1 article (08/2009)|
|4.||Pulgar, Victor M: 1 article (08/2009)|
|5.||Jessup, Jewell A: 1 article (08/2009)|
|6.||Massmann, Angela G: 1 article (08/2009)|
|7.||Reis, A M: 1 article (03/2002)|
|8.||Coimbra, C C: 1 article (03/2002)|
|9.||Machado, L J C: 1 article (03/2002)|
|1.||Hypertension (High Blood Pressure)
05/17/1988 - "These data encourage the use of sarthran as a valuable pharmacological probe in the examination of the role of the brain renin-angiotensin system in hypertension."
12/23/1985 - "The failure of i.c.v. sarthran infusion to block chronic i.v. AII-induced hypertension probably reflects the inability of i.c.v. sarthran to gain access to a critical brain site(s) at which i.v. AII acts to cause increased arterial pressure."
12/23/1985 - "Continuous blockade of brain AII receptors with i.c.v. sarthran had no effect on the ultimate development of hypertension seen in response to 5-day i.v. AII infusion (10 or 20 ng/min) coupled with high sodium intake. "
03/01/1987 - "The present experiments were designed to elucidate the role of central angiotensin II (AII) mechanisms in maintenance of established hypertension in adult spontaneously hypertensive rats (SHR) by determining the blood pressure response to chronic intraventricular (i.v.t.) infusion of the converting enzyme inhibitor teprotide or the AII receptor antagonist 1sar,8Thr-AII (sarthran). "
03/01/2002 - "However, sarthran infusion into adrenodemedullated rats completely blocked this increased prolactin secretion in response to hemorrhage (P<0.01). "
12/07/1995 - "Sarthran infusion into guanethidine-treated rats caused a further 34% decrease in hyperglycemic response to hemorrhage (P < 0.01). "
03/01/2002 - "This increased prolactin secretion in response to hemorrhage observed in guanethidine-treated rats was completely blocked by sarthran preinfusion (P<0.01). "
12/07/1995 - "However, sarthran infusion into adrenodemedullated rats caused a 38.5% further decrease in hyperglycemic response to hemorrhage (P < 0.01); and (3) intact animals submitted to blockade of sympathetic noradrenergic pathways by treatment with guanethidine (10 mg/100 g b.wt.), which greatly decreased the baseline value of plasma glucose (64.1 +/- 3.5 mg% vs. 125.3 +/- 4.5 mg%, P < 0.01), and reduced the hyperglycemic response to hemorrhage by 34% (P < 0.01). "
12/07/1995 - "The animals were divided into 3 experimental groups; (1) sham-operated animals submitted to intravenous administration of [1-Sar,8-Thr]-angiotensin II (sarthran), an antagonist of angiotensin II (750 ng/100 g b.wt. as a bolus plus an infusion of 25 ng/100 g b.wt./min over 30 min), which greatly attenuated (51.8% lower than controls; P < 0.01) the hyperglycemic response to hemorrhage; (2) animals submitted to adrenodemedullation which decreased the hyperglycemic response to hemorrhage by 64% (P < 0.01). "
08/01/1995 - "The effect of preblocking either the AT1 or the AT2 receptors on the sarthran-induced bradycardia was also determined. "
04/01/1991 - "Intracerebroventricular administration of sarthran had no effect on basal blood pressure or heart rate but enhanced the bradycardia in response to increases in MAP in both untreated and captopril-treated rats. "
|5.||Hypotension (Low Blood Pressure)
08/01/1997 - "When Ang-(1-7) (20, 80, and 380 nmol per rat I.A.) was given during bradykinin infusion, it elicited hypotension at 80 and 380 nmol (deltaMAP: -15+/-2.7 and -21+/-3.3 mmHg, respectively; P<.001); this hypotension was not affected by the angiotensin type 1 antagonist L-158,809 (200 microg/kg I.A.), the angiotensin type 2 antagonist PD 123319 (10 mg/kg I.A.), saralasin, or sarthran (10 microg/kg per minute). "
|4.||salicylhydroxamic acid (SHAM)
|5.||Type 1 Angiotensin Receptor
|6.||Type 2 Angiotensin Receptor
|9.||Saralasin (Saralasin Acetate)