Efectos hipotal&aacute;micos de la angiotensina-[1-7] en ratas con coartaci&oacute;n a&oacute;rtica <span class="so-article-trans-title" dir="auto"> Translated title: Hypothalamic Effects of Angiotensin (1-7) in Rats with Aortic Coarctation </span>

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Abstract

El objetivo del presente trabajo fue evaluar el efecto de la administración intrahipotalámica de la angiotensina-[1-7] (Ang-[1-7]) sobre la presión arterial y la frecuencia cardíaca y sobre la actividad presora de la angiotensina II (Ang-II) en ratas con operación simulada (OS) o con coartación aórtica (CoAo) en un estadio temprano y en uno crónico de la hipertensión. Se utilizaron ratas Wistar. A los 7 y 42 días de la operación correspondiente se canuló una arteria carótida para la medición de la presión arterial media (PAM) en ratas anestesiadas y se insertó una aguja inyectora en el hipotálamo anterior para la administración de Ang-II (50 ng), Ang-[1-7] (50 ng) y Ang-II + Ang-[1-7] (50 + 50 ng). La administración hipotálamica de Ang-II produjo un aumento de la PAM en las ratas CoAo con respecto al grupo control en los estadios temprano y crónico de hipertensión, mientras que la Ang-[1-7] no indujo cambios significativos en todos los grupos experimentales. La coadministración de Ang-[1-7] redujo la actividad presora de la Ang-II en las ratas CoAo, mientras que careció de efecto sobre la actividad presora de la Ang-II en las ratas normotensas. En conclusión, la actividad presora de la Ang-II está aumentada en ratas en los estadios temprano y crónico de hipertensión arterial, mientras que el efecto antagónico de la Ang-[1-7] indicaría que ésta modularía la actividad presora de la angiotensina II cuando la Ang-II estuviera exacerbada, ya que se ha observado únicamente en el grupo de ratas hipertensas.

Translated abstract

The objective of the present study was to evaluate the effect of the intrahypothalamic administration of angiotensin-[1-7] (Ang-[1-7]) on blood pressure and heart rate and on angiotensin II (Ang-II) activity in rats with sham operation (SO) and rats with aortic coarctation (ACo) in early and chronic stage of hypertension. Wistar rats were used. Seven and 42 days after the corresponding operation one carotid artery was cannulated for the measurement of the mean arterial pressure (MAP) in anaesthetized rats and an injection needle was inserted in the anterior hypothalamus by means of a stereotactic frame for the administration of Ang-II (50 ng), Ang-[1-7] (50 ng) and Ang-II + Ang-[1-7] (50 + 50 ng). Hypothalamic administration of Ang-II produced an increased MAP in the ACo rats when compared to the control group in the early and chronic stages of hypertension, whereas Ang-[1-7] did not induce significant changes in any experimental group. The co-administration of Ang -[1-7] reduced the pressure activity of the Ang-II in both early and chronic stages of hypertension in the ACo rats, whereas it had no effect on the pressure activity of Ang-II in the normotensive rats. In conclusion, the pressure activity of Ang-II is increased in rats with early and chronic stages of arterial hypertension. The antagonistic effect of Ang-[1-7] may indicate that this peptide could modulate the pressure activity of an already increased Ang-II, since it has been only observed in the hypertensive rats.

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Release of vasopressin from the rat hypothalamo-neurohypophysial system by angiotensin-(1-7) heptapeptide.

C. Ferrario, M Khosla, K Brosnihan … (1988)

We have recently shown that hydrolysis of labeled angiotensin I in canine brainstem homogenate causes a rapid accumulation of the heptapeptide angiotensin-(1-7) [Ang-(1-7)]. Although this angiotensin fragment has no vasopressor activity, its consistent generation in brain homogenate led us to study its potential neurosecretory effects in the rat hypothalamo-neurohypophysial system (HNS) in vitro. Ang-(1-7) or angiotensin II (Ang II) was added to HNS perifusate in concentrations of 0.04, 0.4, and 4 microM, and release of arginine vasopressin (AVP) during each treatment was quantified as a percentage of the AVP release detected in the preceding collection period. Base-line release of AVP averaged 281 +/- 47 pg per 15 min (mean +/- SEM) in HNS explants (five experiments, five explants per chamber) perifused in Krebs solution at 37 degrees C, after a 1-hr equilibration period. At 0.04 microM, Ang II or Ang-(1-7) did not stimulate AVP release. Ang II increased AVP release over the control value by 172% +/- 44% and 268% +/- 66% at 0.4 and 4 microM, respectively; the same concentrations of Ang-(1-7) increased AVP release by 134% +/- 12% and 216% +/- 45%. The responses to Ang II and Ang-(1-7) at the highest concentration were both significant (P less than 0.05), and comparison by two-way analysis of variance indicated that Ang II and Ang-(1-7) were equipotent in stimulating AVP release over the range of concentrations studied. In the presence of the competitive Ang II antagonist [Sar1,Thr8]Ang II (20 microM), the release of AVP increased approximately equal to 2-fold. Neither Ang II nor Ang-(1-7) (4 microM) caused a further enhancement of AVP release in the presence of [Sar1,Thr8]Ang II. These data suggest that a hydrophobic residue in position 8 of the angiotensin peptide is not essential for activation of angiotensin receptors in the rat HNS. Moreover, the equipotence of Ang II and Ang-(1-7) indicates that Ang-(1-7) may participate in the control of AVP release.

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Counterregulatory actions of angiotensin-(1-7).

Debra I. Diz, C. Ferrario, E A Tallant … (1997)

Angiotensin (Ang)-(1-7) is a bioactive component of the renin-angiotensin system that is formed endogenously from either Ang I or Ang II. The first actions described for Ang-(1-7) indicated that the peptide mimicked some of the effects of Ang II, including the release of prostanoids and vasopressin. However, Ang-(1-7) is devoid of vasoconstrictor, central pressor, or thirst-stimulating actions. In fact, new findings reveal depressor, vasodilator, and antihypertensive actions that may be more apparent in hypertensive animals or humans. Thus, the accumulating evidence suggests that Ang-(1-7) may oppose the actions of Ang II either directly or by stimulation of prostaglandins and nitric oxide. These observations are significant because they may explain the effective antihypertensive action of converting enzyme inhibitors in a variety of non-renin-dependent models of experimental and genetic hypertension as well as most forms of human hypertension. In this context, studies in humans and animals showed that the antihypertensive action of converting enzyme inhibitors correlated with increases in plasma levels of Ang-(1-7). In this review, we summarize our knowledge of the mechanisms accounting for the counterregulatory actions of Ang-(1-7) and elaborate on the emerging concept that Ang-(1-7) functions as an antihypertensive peptide within the cascade of the renin-angiotensin system.