Ontogeny of baroreflex control of renal sympathetic nerve activity and heart rate

1992 ◽  
Vol 263 (6) ◽  
pp. H1819-H1826 ◽  
Author(s):  
J. L. Segar ◽  
G. Hajduczok ◽  
B. A. Smith ◽  
D. C. Merrill ◽  
J. E. Robillard
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Baroreflex Function ◽  
Baroreceptor Stimulation ◽  
Renal Sympathetic

The purpose of this study was to characterize the developmental changes in baroreflex function during fetal and postnatal life in sheep. Resting mean arterial blood pressure increased significantly from 55 +/- 2 mmHg in fetuses to 86 +/- 3 mmHg in newborn lambs and to 105 +/- 4 mmHg in 4- to 6-wk-old lambs. The sensitivity (gain) of the renal sympathetic nerve activity (RSNA) response to baroreceptor stimulation was greater (P < 0.05) in fetuses (-7.7 +/- 1.9%/mmHg) than in newborn (-2.9 +/- 0.1%/mmHg) and 4- to 6-wk-old lambs (-2.2 +/- 0.2%/mmHg). The threshold and saturation pressures for the baroreflex function curve were lower (P < 0.05) in fetuses (44 +/- 2 and 61 +/- 2 mmHg) than in newborn (59 +/- 4 and 106 +/- 5 mmHg) or 4- to 6-wk-old lambs (78 +/- 5 and 132 +/- 6 mmHg). Similar findings were observed when the heart rate response to baroreceptor stimulation was examined. Additional experiments were performed in newborn and 4- to 6-wk-old lambs to determine whether the rise in arterial blood pressure associated with postnatal maturation contributed to baroreflex resetting. Sustained elevation of arterial blood pressure by 15–20 mmHg for over 90 min did not reset the baroreflex function curve in either newborn or 4- to 6-wk-old lambs.(ABSTRACT TRUNCATED AT 250 WORDS)

Nitric oxide within the paraventricular nucleus mediates changes in renal sympathetic nerve activity

1997 ◽  
Vol 273 (3) ◽  
pp. R864-R872 ◽  
Author(s):  
K. Zhang ◽  
W. G. Mayhan ◽  
K. P. Patel
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Renal Sympathetic

The paraventricular nucleus (PVN) of the hypothalamus is known to be involved in the control of sympathetic outflow. The goal of the present study was to examine the role of nitric oxide within the PVN in the regulation of renal sympathetic nerve activity. Renal sympathetic nerve discharge (RSND), arterial blood pressure, and heart rate in response to the microinjection of nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA; 50, 100, and 200 pmol) into the PVN were measured in male Sprague-Dawley rats. Microinjection of L-NMMA elicited an increase in RSND, arterial blood pressure, and heart rate. Administration of NG-monomethyl-D-arginine (D-NMMA, 50-200 pmol) into the PVN did not change RSND, arterial pressure, or heart rate. Similarly, microinjection of another nitric oxide inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 100 nmol) also elicited an increase in RSND, arterial blood pressure, and heart rate. L-Arginine (100 nmol) reversed the effects of L-NAME in the PVN. Furthermore, microinjection of sodium nitroprusside (SNP; 50, 100, and 200 nmol) into the PVN elicited a significant decrease in RSND, arterial blood pressure, and heart rate. These effects of L-NMMA, L-NAME, and SNP on RSND and arterial blood pressure were not mediated by their vasoactive action because microinjection of phenylephrine and hydralazine did not elicit similar respective changes. In conclusion, our data indicate that endogenous nitric oxide within the PVN regulates sympathetic outflow via some inhibitory mechanisms. Altered nitric oxide mechanisms within the PVN may contribute to elevated sympathetic nerve activity observed during various diseases states such as heart failure and hypertension.

Acute inhibition of the hypothalamic paraventricular nucleus decreases renal sympathetic nerve activity and arterial blood pressure in water-deprived rats

2004 ◽  
Vol 286 (4) ◽  
pp. R719-R725 ◽  
Author(s):  
Sean D. Stocker ◽  
Kimberly J. Keith ◽  
Glenn M. Toney
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Renal Sympathetic

The present study was performed to determine whether sympathetic outflow and arterial blood pressure in water-deprived rats are dependent on the ongoing neuronal activity of the hypothalamic paraventricular nucleus (PVN). Renal sympathetic nerve activity (RSNA), mean arterial blood pressure (MAP), and heart rate were recorded in urethane-α-chloralose-anesthetized rats that were deprived of water but not food for 48 h before experiments. Acute inhibition of the PVN by bilateral microinjection of the GABAA agonist muscimol (100 pmol/side) significantly decreased RSNA in water-deprived rats (-26.7 ± 4.7%, n = 7) but was without effect in control rats (1.3 ± 6.3%, n = 7). Similarly, injection of muscimol produced a greater decrease in MAP in water-deprived rats than in control rats (-46 ± 3 vs. -16 ± 3 mmHg, respectively), although baseline MAP was not different between groups (105 ± 4 vs. 107 ± 4 mmHg, respectively). Neither bilateral microinjection of isotonic saline vehicle (100 nl/side) into the PVN nor muscimol (100 pmol/side) outside the PVN altered RSNA or MAP in either group. In addition, ganglionic blockade with hexamethonium (30 mg/kg iv) significantly decreased MAP in both groups; however, the decrease in MAP was significantly greater in water-deprived rats than in control rats (62 ± 2 vs. 48 ± 2 mmHg, respectively). Collectively, these findings suggest that sympathetic outflow contributes more to the maintenance of blood pressure in the water-deprived rat, and this depends, at least partly, on the ongoing activity of PVN neurons.

Are prostaglandins involved in atrial natriuretic peptide mechanisms of cardiovascular control?

1999 ◽  
Vol 77 (3) ◽  
pp. 211-215 ◽  
Author(s):  
Karim S Bandali ◽  
Uwe Ackermann
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Prostaglandin Synthesis ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Renal Sympathetic

Atrial natriuretic peptide (ANP) can excite cardiac nerve endings and invoke a decrease in arterial blood pressure and a reduction in renal sympathetic nerve activity. Our laboratory has previously demonstrated that this renal depressor reflex was invoked by systemic injection of ANP and not by the direct application of ANP to the epicardium, a major locus for vagal afferents. We now examine whether inhibition of prostaglandin synthesis impairs reflex responses that are normally associated with ANP injections. Renal sympathetic nerve activity, arterial blood pressure, and heart rate were recorded in anesthetized rats. Indomethacin was used to inhibit prostaglandin synthesis through the cyclooxygenase pathway. The ANP-mediated decrease in arterial blood pressure and renal sympathetic nerve activity, observed when prostaglandin synthesis was inhibited, did not differ significantly from the decreases observed in these parameters when prostaglandin synthesis was not inhibited. Heart rate remained unchanged. Our results suggest that the sympatho-inhibitory effects of ANP do not require prostaglandins as intermediary compounds.Key words: sympathetic nervous system, renal nerves, prostaglandins.

Interactions between ANP and ANG II in regulating blood pressure and sympathetic outflow

1991 ◽  
Vol 260 (6) ◽  
pp. R1145-R1151 ◽  
Author(s):  
M. K. Steele ◽  
D. G. Gardner ◽  
P. L. Xie ◽  
H. D. Schultz
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Contrast Injection ◽  
Synthesis Inhibitor ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Renal Sympathetic

In anesthetized rats with sinoaortic denervation, intracerebroventricular (icv) injection of atrial natriuretic peptide (ANP) resulted in decreased mean arterial blood pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) (depressor effects), whereas icv angiotensin II (ANG II) produced increases in these variables (pressor effects). The depressor effects of ANP were slower in onset and longer in duration than the pressor effects of ANG II. Intracerebroventricular injection of the ANG II-receptor blocker sarthran or the ANG II-synthesis inhibitor captopril resulted in a significant reduction in MAP; HR and RSNA were not affected. Both sarthran and captopril abolished the depressor responses to icv ANP. In contrast, injection of an anti-rat ANP antibody, which blocked the depressor effects of icv ANP, did not by itself modify MAP, HR, or RSNA, nor did the antibody affect the pressor responses to icv ANG II. These data suggest that, in this animal model, the depressor effects of icv ANP are mediated by the inhibition of brain ANG II-dependent neural activity. These results also demonstrate that, in this preparation, the endogenous ANG II system actively contributes to the maintenance of basal MAP, whereas the central ANP system, at least in regions accessible to the antirat ANP antibody, plays little role in this maintenance.

Baroreflex control of muscle sympathetic nerve activity during skin surface cooling

2007 ◽  
Vol 103 (4) ◽  
pp. 1284-1289 ◽  
Author(s):  
Jian Cui ◽  
Sylvain Durand ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Skin Surface ◽  
Surface Cooling ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Arterial Blood

Skin surface cooling improves orthostatic tolerance through a yet to be identified mechanism. One possibility is that skin surface cooling increases the gain of baroreflex control of efferent responses contributing to the maintenance of blood pressure. To test this hypothesis, muscle sympathetic nerve activity (MSNA), arterial blood pressure, and heart rate were recorded in nine healthy subjects during both normothermic and skin surface cooling conditions, while baroreflex control of MSNA and heart rate were assessed during rapid pharmacologically induced changes in arterial blood pressure. Skin surface cooling decreased mean skin temperature (34.9 ± 0.2 to 29.8 ± 0.6°C; P < 0.001) and increased mean arterial blood pressure (85 ± 2 to 93 ± 3 mmHg; P < 0.001) without changing MSNA ( P = 0.47) or heart rate ( P = 0.21). The slope of the relationship between MSNA and diastolic blood pressure during skin surface cooling (−3.54 ± 0.29 units·beat−1·mmHg−1) was not significantly different from normothermic conditions (−2.94 ± 0.21 units·beat−1·mmHg−1; P = 0.19). The slope depicting baroreflex control of heart rate was also not altered by skin surface cooling. However, skin surface cooling shifted the “operating point” of both baroreflex curves to high arterial blood pressures (i.e., rightward shift). Resetting baroreflex curves to higher pressure might contribute to the elevations in orthostatic tolerance associated with skin surface cooling.

Sign in / Sign up

Export Citation Format

Share Document