Why the study?
Does acute intravenous ethanol affect baroreceptor reflex control of heart rate differently in spontaneously hypertensive rats compared to normotensive rats?
Does acute intravenous ethanol affect baroreceptor reflex control of heart rate differently in spontaneously hypertensive rats compared to normotensive rats?
Acute intravenous ethanol attenuates baroreceptor reflex sensitivity in normotensive rats but not in spontaneously hypertensive rats, while producing a brief pressor effect in both.
Hypothesis-generating for differential ethanol effects on baroreflex by hypertension status; human studies needed before any clinical consideration.
This study investigated the acute effects of ethanol (0.25, 0.5, or 1 g/kg, iv) on mean arterial pressure, heart rate, and gain of the baroreceptor reflex control of heart rate (BRS) in conscious spontaneously hypertensive rats (SHRs) and age‐matched Wistar rats. BRS was substantially lower in the SHRs as compared with the Wistar rats when measured by phenylephrine (‐0.95 ± 0.16 vs. ‐2.02 ± 0.22 beats/min/mm Hg) or nitroprusside (‐1.90 ± 0.2 vs. ‐3.02 ± 0.32 beats/min/mm Hg). None of the doses of ethanol influenced BRS in the SHR. In contrast, ethanol attenuated BRS in Wistar rats, but this effect was dependent on the dose used and the type of response. The lower doses attenuated the reflex tachycardic response, but had no effect on the reflex bradycardic response. On the other hand, the 1 g/kg dose of ethanol attenuated the reflex bradycardic but not the tachycardic response. Ethanol produced a pressor effect (15‐25 mm Hg; 5‐min duration), which was neither dose‐ nor strain‐dependent. However, only in the SHR mean arterial pressure remained elevated (10‐15 mm Hg above control) for 20 min in response to the 0.5 g/kg dose of ethanol, and its recovery coincided with the occurrence of a slowly developing negative chronotropic response. Ethanol produced a dose‐related negative chronotropic effect in both strains of rats that was of longer duration in the SHR, particularly with the 1 g/kg dose. It is possible that the bradycardic effect of ethanol influenced negatively its pressor effects. Data suggest that, in conscious rats, ethanol: (1) attenuates BRS in normotensive rats but not in the SHR; (2) causes a brief pressor effect that is not related to its dose, the level of arterial pressure, or its influence on the gain of the baroreceptor reflex; and (3) elicits dose‐related bradycardic responses that are of longer duration in the SHR, particularly with the higher dose. This negative chronotropic effect of ethanol may limit its pressor effect in SHRs.
No takes yet. Share an insight, caveat, or question.
Abdel A. Abdel‐Rahman (1994) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: