INVESTIGADORES
GIRONACCI Mariela Mercedes
artículos
Título:
Anterior hypothalamic β-adrenoceptors in chronic aortic coarctated hypertensive rats. An interaction with central angiotensin II receptors.
Autor/es:
C HÖCHT, JAW OPEZZO, MM GIRONACCI, C PEÑA, CA TAIRA
Revista:
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
Referencias:
Año: 2005 p. 30 - 34
ISSN:
0305-1870
Resumen:
1. The aim of the
present study was to investigate the activity of anterior hypothalamic β-adrenoceptors
and angiotensin (Ang) II receptors on blood pressure in normotensive rats and
aortic-coarctated (ACo) animals at a chronic stage of hypertension. A possible
interaction between β-adrenoceptors and AngII pressor activity was also
investigated.
2. Injection of
isoproterenol (0.1?10 nmol) in the anterior hypothalamic area induced a
dose-dependent decrease in mean arterial pressure (MAP) in sham-operated (SO),
but not in ACo, animals. Isoproterenol (1 nmol) reduced blood pressure in SO
rats (∆MAP ?10.1+0.4 mmHg; n= 10) but not in
ACo animals (∆MAP ?0.9+1.6 mmHg; n= 10; P< 0.05 vs SO rats). Whereas
previous administration of atenolol (40 nmol) enhanced the cardiovascular
effect of isoproterenol (1 nmol) in ACo rats but not in SO animals, propranolol
(40 nmol) prevented the hypotensive action of isoproterenol in both experimental
groups. Intrahypothalamic administration of clenbuterol decreased MAP in a
dose-dependent manner; however, the depressor response to clenbuterol (10 nmol)
was greater in ACo rats than in SO rats (∆MAP ?26.8+3.2 vs ?14.4+2.4
mmHg, respectively; n= 5 for both; P< 0.05). When
AngII (50 ng) was injected into the anterior hypothalamic area, a greater
pressor response was observed in ACo rats than in SO rats (∆MAP 19.6+1.1
vs 11.3 +0.6 mmHg, respectively; n= 5 for both; P< 0.05).
Atenolol (40 nmol) pretreatment partially and significantly prevented the pressor
response to AngII in ACo rats, but not in SO rats.
3. In conclusion, these results provide
pharmacological evidence for the existence of a β1-adrenoceptor-mediatedpressor mechanism
in the anterior hypothalamic area of ACo rats that is absent in SO rats. The
enhanced depressor β2-adrenoceptor activity observed in chronic ACo rats could be a
compensatory adjustment to pressor β1-adrenoceptor activity. Conversely, pressor
overactivity of AngII was observed in the anterior hypothalamic area of ACo
rats at a chronic hypertensive stage; this enhancement could be explained, at
least in part, by the pressor β1-adrenoceptor activity.