bq-123 has been researched along with Ventricular-Dysfunction--Left* in 3 studies
1 trial(s) available for bq-123 and Ventricular-Dysfunction--Left
| Article | Year |
|---|---|
Short-term haemodynamic effects of BQ-123, a selective endothelin ET(A)-receptor antagonist, in chronic heart failure.
Topics: Endothelin Receptor Antagonists; Heart Failure; Hemodynamics; Humans; Peptides, Cyclic; Time Factors; Vascular Resistance; Ventricular Dysfunction, Left | 1998 |
2 other study(ies) available for bq-123 and Ventricular-Dysfunction--Left
| Article | Year |
|---|---|
Activation of endothelin A receptors contributes to impaired responsiveness of renal mechanosensory nerves in congestive heart failure.
Increasing renal pelvic pressure results in PGE2-mediated release of substance P, leading to increases in afferent renal nerve activity (ARNA) and natriuresis, that is, a renorenal reflex response. The renorenal reflexes are impaired in congestive heart failure (CHF). Impairment of the renorenal reflexes may contribute to the increased renal sympathetic nerve activity and sodium retention in CHF. Endothelin (ET)-1 contributes to the pathological changes in cardiac and renal function in CHF. Therefore, we examined whether the ETA receptor antagonist BQ123 altered the responsiveness of renal mechanosensory nerves in CHF. The ARNA responses to increasing renal pelvic pressure were suppressed in CHF but not in sham-CHF rats. In CHF, increasing renal pelvic pressure by 7.5 mm Hg before and during renal pelvic perfusion with BQ123 increased ARNA 12% +/- 3% and 21% +/- 3% (p < 0.05 vs. vehicle). In isolated renal pelvises from CHF rats, PGE2 increased substance P release from 5 +/- 0 to 7 +/- 1 pg/min without BQ123 and from 4 +/- 1 to 9 +/- 1 pg/min with BQ123 in the bath (p < 0.01 vs. vehicle). BQ123 had no effect on the ARNA responses or substance P release in sham-CHF. In conclusion, activation of ETA receptors contributes to the impaired responsiveness of renal mechanosensory nerves in CHF rats by a mechanism(s) at the renal sensory nerve endings. Topics: Afferent Pathways; Animals; Antihypertensive Agents; Dinoprostone; Disease Models, Animal; Endothelin A Receptor Antagonists; Heart Failure; Hydrostatic Pressure; Kidney; Kidney Pelvis; Male; Mechanoreceptors; Myocardium; Organ Size; Peptides, Cyclic; Perfusion; Rats; Rats, Sprague-Dawley; Receptor, Endothelin A; Sodium; Substance P; Ventricular Dysfunction, Left | 2010 |
Modulation of renal blood flow by endogenous endothelin-1 in conscious rabbits with left ventricular dysfunction.
The current study addresses the functional status and role of the endothelin ET(A) receptor for renal vascular function in rabbits with and without heart failure (epinephrine-induced cardiomyopathy). Under baseline conditions, the ET(A) receptor antagonist BQ-123 did not change basal renal hemodynamics, but completely prevented endothelin-1 (ET-1)-induced renal vasoconstriction. In heart failure, in the presence of elevated plasma ET-1 concentrations (P < .05), renal vasoconstriction in response to exogenous ET-1 was intact. Unlike under baseline conditions, ET(A) receptor antagonism markedly increased renal blood flow (P <.05) and decreased renal vascular resistance (P < .05) in heart failure. The current study provides new insight into the pathophysiology of renal vasoconstriction associated with heart failure and the specific role of the renal ET(A) receptor in this pathophysiologic adaptation. Topics: Adrenergic Agonists; Animals; Cardiac Output, Low; Chinchilla; Endothelin Receptor Antagonists; Endothelin-1; Epinephrine; Hemodynamics; Male; Neurotransmitter Agents; Peptides, Cyclic; Rabbits; Receptor, Endothelin A; Receptors, Endothelin; Renal Circulation; Vasoconstriction; Ventricular Dysfunction, Left | 1999 |