Effects of pregnancy and progesterone metabolites on arterial baroreflex in conscious rats

1997 ◽  
Vol 272 (3) ◽  
pp. R924-R934 ◽  
Author(s):  
S. Masilamani ◽  
C. M. Heesch

Previous experiments in anesthetized rats suggested that sympathoexcitatory responses were attenuated in pregnant (P) rats. The major progesterone metabolite, 3alpha-hydroxy-dihydroprogesterone (3alpha-OH-DHP), is elevated in pregnancy and reportedly potentiates central gamma-aminobutyric acidergic mechanisms, whereas the 3beta-isomer (3beta-OH-DHP) is inactive. This study obtained baroreflex curves in conscious rats by recording reflex changes in renal sympathetic nerve activity (RSNA) and heart rate (HR) due to perturbations in mean arterial pressure (MAP) [i.v. phenylephrine (PE) and nitroprusside (NTP)] in P rats and in virgin (V) rats before (control) and 15 min after infusion (i.v.) of 3alpha-OH-DHP or 3beta-OH-DHP. Baseline MAP was lower in P rats (P = 102 +/- 2 vs. V = 124 +/- 3 mmHg). Compared with V rats, P rats exhibited less "sympathetic reserve" to respond to a hypotensive challenge, as evidenced by decreased maximum NA and decreased slope of RSNA baroreflex responses to NTP. However, HR baroreflex curves were similar in P and V rats. Acute intravenous administration of 3alpha-OH-DHP to conscious V rats mimicked the effects of pregnancy. Baroreflex sympathoexcitatory responses were decreased, whereas baroreflex control of HR was unaffected. The 3beta-isomer of DHP had no effect on NA or HR baroreflex responses. These results suggest that pregnancy may have differential effects on baroreflex control of sympathetic outflow and HR, and the major metabolite of progesterone, 3alpha-OH-DHP, may contribute to this adaptation of pregnancy.


2008 ◽  
Vol 295 (1) ◽  
pp. R8-R14 ◽  
Author(s):  
Roy Kanbar ◽  
Bruno Chapuis ◽  
Valérie Oréa ◽  
Christian Barrès ◽  
Claude Julien

This study compared the baroreflex control of lumbar and renal sympathetic nerve activity (SNA) in conscious rats. Arterial pressure (AP) and lumbar and renal SNA were simultaneously recorded in six freely behaving rats. Pharmacological estimates of lumbar and renal sympathetic baroreflex sensitivity (BRS) were obtained by means of the sequential intravenous administration of sodium nitroprusside and phenylephrine. Sympathetic BRS was significantly ( P < 0.05) lower for lumbar [3.0 ± 0.4 normalized units (NU)/mmHg] than for renal (7.6 ± 0.6 NU/mmHg) SNA. During a 219-min baseline period, spontaneous lumbar and renal BRS were continuously assessed by computing the gain of the transfer function relating AP and SNA at heart rate frequency over consecutive 61.4-s periods. The transfer gain was considered only when coherence between AP and SNA significantly differed from zero, which was verified in 99 ± 1 and 96 ± 3% of cases for lumbar and renal SNA, respectively. When averaged over the entire baseline period, spontaneous BRS was significantly ( P < 0.05) lower for lumbar (1.3 ± 0.2 NU/mmHg) than for renal (2.3 ± 0.3 NU/mmHg) SNA. For both SNAs, spontaneous BRS showed marked fluctuations (variation coefficients were 26 ± 2 and 28 ± 2% for lumbar and renal SNA, respectively). These fluctuations were positively correlated in five of six rats ( R = 0.44 ± 0.06; n = 204 ± 8; P < 0.0001). We conclude that in conscious rats, the baroreflex control of lumbar and renal SNA shows quantitative differences but is modulated in a mostly coordinated way.



2002 ◽  
Vol 282 (5) ◽  
pp. H1592-H1602 ◽  
Author(s):  
Max G. Sanderford ◽  
Vernon S. Bishop

Short-term intravenous infusion of angiotensin II (ANG II) into conscious rabbits reduces the range of renal sympathetic nerve activity (RSNA) by attenuating reflex disinhibition of RSNA. This action of ANG II to attenuate the arterial baroreflex range is exaggerated when ANG II is directed into the vertebral circulation, which suggests a mechanism involving the central nervous system. Because an intact area postrema (AP) is required for ANG II to attenuate arterial baroreflex-mediated bradycardia and is also required for maintenance of ANG II-dependent hypertension, we hypothesized that attenuation of maximum RSNA during infusion of ANG II involves the AP. In conscious AP-lesioned (APX) and AP-intact rabbits, we compared the effect of a 5-min intravenous infusion of ANG II (10 and 20 ng · kg−1 · min−1) on the relationship between mean arterial blood pressure (MAP) and RSNA. Intravenous infusion of ANG II into AP-intact rabbits resulted in a dose-related attenuation of maximum RSNA observed at low MAP. In contrast, ANG II had no effect on maximum RSNA in APX rabbits. To further localize the central site of ANG II action, its effect on the arterial baroreflex was assessed after a midcollicular decerebration. Decerebration did not alter arterial baroreflex control of RSNA compared with the control state, but as in APX, ANG II did not attenuate the maximum RSNA observed at low MAP. The results of this study indicate that central actions of peripheral ANG II to attenuate reflex disinhibition of RSNA not only involve the AP, but may also involve a neural interaction rostral to the level of decerebration.



2015 ◽  
Vol 309 (2) ◽  
pp. R169-R178 ◽  
Author(s):  
Maximilian I. Pinkham ◽  
Gillian A. Whalley ◽  
Sarah-Jane Guild ◽  
Simon C. Malpas ◽  
Carolyn J. Barrett

There is controversy regarding whether the arterial baroreflex control of renal sympathetic nerve activity (SNA) in heart failure is altered. We investigated the impact of sex and ovarian hormones on changes in the arterial baroreflex control of renal SNA following a chronic myocardial infarction (MI). Renal SNA and arterial pressure were recorded in chloralose-urethane anesthetized male, female, and ovariectomized female (OVX) Wistar rats 6–7 wk postsham or MI surgery. Animals were grouped according to MI size (sham, small and large MI). Ovary-intact females had a lower mortality rate post-MI (24%) compared with both males (38%) and OVX (50%) ( P < 0.05). Males and OVX with large MI, but not small MI, displayed an impaired ability of the arterial baroreflex to inhibit renal SNA. As a result, the male large MI group (49 ± 6 vs. 84 ± 5% in male sham group) and OVX large MI group (37 ± 3 vs. 75 ± 5% in OVX sham group) displayed significantly reduced arterial baroreflex range of control of normalized renal SNA ( P < 0.05). In ovary-intact females, arterial baroreflex control of normalized renal SNA was unchanged regardless of MI size. In males and OVX there was a significant, positive correlation between left ventricle (LV) ejection fraction and arterial baroreflex range of control of normalized renal SNA, but not absolute renal SNA, that was not evident in ovary-intact females. The current findings demonstrate that the arterial baroreflex control of renal SNA post-MI is preserved in ovary-intact females, and the state of left ventricular dysfunction significantly impacts on the changes in the arterial baroreflex post-MI.





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