The present study investigates the baroreceptor reflex control of heart rate (HR) of normotensive male and female human volunteers under two conditions: bolus- and infusion-evoked elevations of blood pressure by intravenous administration of phenylephrine. Average age and blood pressure were similar in both sexes, but females had a significantly lower heart period (HP; higher HR). A major difference existed between the two sexes when the blood pressure was elevated by the bolus method. Females had a significantly (50%) smaller baroreflex sensitivity (regression coefficient), which inferred a gender-related difference in baroreceptor reflex control of HR. However, because a positive correlation existed between basal HP and baroreflex sensitivity, it was important to investigate whether this difference was related to the significantly lower basal HP in females. This possibility was ruled out because a similar difference still existed when the data were collected from another group of females who had basal HP values similar to those of males. This gender-related difference in baroreceptor reflex control of HR seems to depend on the pattern by which the pressor stimulus is evoked. The baroreceptor HP response to a slowly developing pressor response that was maintained at a steady-state level was very similar in both sexes. Because the HP response to abrupt (bolus-evoked) pressor stimuli mainly reflects the activity of the vagal component, our findings suggest that the cardiac vagal component seems to play a substantially smaller role in the baroreflex-mediated bradycardia in females.

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Objective: Estrogen exerts a wide variety of actions involving many target tissues. We studied the effects of long-term ovariectomy (OVX) and OVX with 17b-estradiol treatment (OVXE2) on the level of estrogen receptor (ER) gene expression in target tissues of female rats. Design: Three groups of Sprague-Dawley female rats were utilized in this study: sham operated (SO), OVX and OVXE2. Methods: SO and OVX were performed 2 weeks before starting the 17b-estradiol treatment. All groups were maintained on liquid diet for 12 weeks from the time of estradiol treatment. Total RNA was prepared from the tissues of the rats and relative quantitative reverse transcription PCR was utilized to compare the ER a-subtype (ERa) mRNA level in the three groups for each target tissue. Results: Following long-term OVX, the levels of ERa expression showed a significant increase in the uterus, kidney and cerebral cortex and no significant change in the liver, cerebellum, brainstem, heart and thoracic and abdominal aorta compared with their SO levels. On the other hand, a 12-week treatment of OVX rats with 17b-estradiol restored the previously upregulated ERa mRNA to near SO levels except for the liver where the 17b-estradiol treatment resulted in a significant increase in the ERa mRNA level compared with that in SO rats. Conclusions: We conclude that the regulation of ERs by its ligand is tissue specific.

The effects of acute ethanol administration on blood pressure, heart rate and the baroreceptor reflex control of heart rate were studied in normotensive subjects who served as their own control. Baroreceptor reflex control of heart rate was measured by two methods: the ramp method and the steady state method. None of the doses of ethanol had any effect on blood pressure during the observation period, except for the highest dose where a slight elevation was evident for a short period of time. On the other hand, the heart rate showed a slight but consistent dose-related increase. In general, ethanol attenuated the baroreceptor mediated bradycardia but this effect was dependent on the way in which blood pressure was elevated. A dose-related impairment of baroreceptors was evident when the ramp method was used, i.e. ethanol significantly depressed baroreflex sensitivity, expressed as delta heart period (HP)/delta mean arterial pressure (MAP). In contrast, delta HP/delta MAP was not influenced by ethanol when the steady state method was used. However, the steady state baroreflex curves were reset about a higher median blood pressure (MAP50), suggesting that the baroreceptors will be operative at higher blood pressure levels after ethanol. The pressor responsiveness was also influenced differently by ethanol depending on the method of injecting phenylephrine. An increase in pressor responsiveness was evident, though not dose-related, after ethanol only when blood pressure was elevated by the ramp method, suggesting that the inverse relationship between baroreflex sensitivity and pressor responsiveness is more prominent with the ramp method and/or when impairment rather than resetting of baroreceptors occurs. That the decrease in baroreflex sensitivity and the increase in MAP50 were related to peak ethanol levels in blood and that the blood pressure was not influenced by ethanol strongly suggest these effects were ethanol mediated. The weakened buffering action of the baroreflexes would be expected to favour the development of higher blood pressure.

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