Navegando por Palavras-chave "ANGIOTENSIN-II"

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    CARDIOVASCULAR EFFECTS PRODUCED BY MICROINJECTION of ANGIOTENSIN-(1-7) ON VASOPRESSOR and VASODEPRESSOR SITES of the VENTROLATERAL MEDULLA
    (Elsevier B.V., 1993-06-11) Silva, LCS; Fontes, MAP; Campagnolesantos, M. J.; Khosla, M. C.; Campos, R. R.; Guertzenstein, P. G.; Santos, RAS; Universidade Federal de Minas Gerais (UFMG); Universidade Federal de São Paulo (UNIFESP); CLEVELAND CLIN EDUC FDN
    In this study, we determined the cardiovascular effects produced by micro-injection of the heptapeptide Angiotensin-(1-7) [Ang-(1-7)] into the rat ventrolateral medulla (VLM). Micro-injection of Ang-(1-7) into the rostral VLM and the caudal pressor area of the VLM produced significant increases in arterial pressure, comparable to that observed with micro-injection of Ang II. the changes in arterial pressure were associated with more variable changes in heart rate (HR) (usually tachycardia). On the other hand, micro-injection of Ang-(1-7) into the caudal depressor area induced decreases in arterial pressure and HR. the results suggest that, besides Ang II, Ang-(1-7) is involved in the mediation of the cardiovascular actions of the renin-angiotensin system in the VLM.
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    Increased intracellular Na+ and depolarization favor angiotension tachyphylaxis in rabbit aorta
    (Amer Physiological Soc, 1991-02-01) Frediani-Neto, Eugenio [UNIFESP]; Silva, Eneida de Gusmão [UNIFESP]; Paiva, Therezinha Bandiera [UNIFESP]; Paiva, Antonio Cechelli de Mattos [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Tachyphylaxis to both angiotensin II (ANG II) and Sar1-ANG II is observed in normal rabbit aorta rings, but helical strips show tachyphylaxis only to Sar1-ANG II, whereas everted rings are not tachyphylactic to either analogue. In normal rings, a good correlation was observed between intraluminal pH and degree of tachyphylaxis to both analogues, suggesting that rate-limiting access of the agonists to their site of action may enhance tachyphylaxis in this preparation. Membrane potential and intracellular Na+ activity measurements, as well as the relaxation by K+ of norepinephrine-contracted preparations in K+-free medium, indicated that helical strips are more depolarized than everted rings due to Na+ leakage into the smooth muscle cells. These results suggest that the differences in the degree of tachyphylaxis induced by angiotensin in different rabbit aorta preparations are due to a less accessible site of action in normal rings and to the higher intracellular Na+ and more depolarized state of helical strips relative to everted rings.
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    ROLE of NA+ and PROTEIN-KINASE-C in ANGIOTENSIN DESENSITIZATION and TACHYPHYLAXIS in the GUINEA-PIG ILEUM
    (Springer, 1993-04-01) Shimuta, S. I.; Kanashiro, C. A.; Ferreira, A. T.; Oshiro, MEM; Paiva, T. B.; Paiva, ACM; Universidade Federal de São Paulo (UNIFESP)
    Simultaneous recordings of the tension and intracellular Ca2+ concentration of guinea-pig ileum longitudinal smooth muscle strips, as well as Na-24+ and Ca-45(2+) influx measurements in cultured myocytes from the same tissue, were used to investigate the mechanisms underlying angiotensin-induced desensitization and tachyphylaxis. Angiotensin II and [2-lysine]-angiotensin II (Lys2All), incubated for prolonged periods (10 min) with muscle strips, induced fading of the contractile response (desensitization) and reappearance of the intracellular Ca2+ concentration oscillations, which were inhibited during the initial increase in cytosolic Ca2+. the desensitization was paralleled, in cultured myocytes, by inhibition of the Ca-45(2+) but not of the Na-24+ influxes which were initially stimulated by the peptides. On the other hand, repeated administrations of angiotensin II (but not of LyS2All) caused gradual reduction of the contractile response and of the Na-24+ influx stimulation evoked by the agonist (tachyphylaxis). Treatment with phorbol 12-13 dibutyrate accelerated the desensitization induced by both angiotensin II and by Lys2All and aggravated the tachyphylaxis to angiotensin II. the results support the hypothesis that activation of protein kinase C is responsible for the desensitization and that tachyphylaxis is due to the slow dissociation of angiotensin II from a postulated Na+-dependent regulatory site on the receptor.