Baroreceptor Reflex Sensitivity Estimated by the Sequence Technique is Reliable in Rats

Stauss, Harald M.; Moffitt, Julia A.; Chapleau, Mark W.; Abboud, François M.; Johnson, Alan Kim

doi:10.1152/ajpheart.00228.2006

Cited by 56 publications

(47 citation statements)

References 8 publications

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“…The slope of the regression line between spontaneous changes in AP and PI values is taken as an index of BRS, as is done when AP and PI changes are induced by vasoactive drug injections (37). The baroreflex nature of the PI/AP sequences has been demonstrated in cats (3), rats (38), and mice (20). This technique is particularly suitable to mice because these animals are not amenable to receive multiple intravenous injections.…”

Section: Discussionmentioning

confidence: 99%

Changes in hemodynamic and neurohumoral control cause cardiac damage in one-kidney, one-clip hypertensive mice

Borges

Salgado

Silva³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Sympathovagal balance and baroreflex control of heart rate (HR) were evaluated during the development (1 and 4 wk) of one-kidney, one-clip (1K1C) hypertension in conscious mice. The development of cardiac hypertrophy and fibrosis was also examined. Overall variability of systolic arterial pressure (AP) and HR in the time domain and baroreflex sensitivity were calculated from basal recordings. Methyl atropine and propranolol allowed the evaluation of the sympathovagal balance to the heart and the intrinsic HR. Staining of renal ANG II in the kidney and plasma renin activity (PRA) were also evaluated. One and four weeks after clipping, the mice were hypertensive and tachycardic, and they exhibited elevated sympathetic and reduced vagal tone. The intrinsic HR was elevated only 1 wk after clipping. Systolic AP variability was elevated, while HR variability and baroreflex sensitivity were reduced 1 and 4 wk after clipping. Renal ANG II staining and PRA were elevated only 1 wk after clipping. Concentric cardiac hypertrophy was observed at 1 and 4 wk, while cardiac fibrosis was observed only at 4 wk after clipping. In conclusion, these data further support previous findings in the literature and provide new features of neurohumoral changes during the development of 1K1C hypertension in mice. In addition, the 1K1C hypertensive model in mice can be an important tool for studies evaluating the role of specific genes relating to dependent and nondependent ANG II hypertension in transgenic mice. renovascular hypertension; sympathetic tone; vagal tone; intrinsic heart rate; baroreflex THE UNDERSTANDING OF THE PATHOPHYSIOLOGY of hypertension has been greatly advanced because of studies performed in several species, including dog, rabbit, and rat (9,12,14). Among the experimental models of hypertension, the renovascular model has brought considerable insights to studies of the pathophysiology of hypertension (4,33,45). In particular, it is well recognized that the onset and development of one-kidney, one clip (1K1C) hypertension have complex mechanisms involving humoral and autonomic aspects.The renin-angiotensin system (RAS) plays a key role in the onset of 1K1C hypertension and its biologically active hormone, ANG II, has important hemodynamic effects, leading to rise in arterial pressure (AP) (9). Studies from our laboratory (24,26) demonstrated that the 1st wk of 1K1C hypertension in rats is accompanied by a transient tachycardia and increased intrinsic heart rate (HR). Other studies performed on 1K1C hypertensive rats have indicated that sympathetic drive is involved in the development and maintenance of this model of hypertension (4, 17). It was observed that 1K1C hypertension is accompanied by an increased cardiac sympathetic drive from the 1st wk after clipping and a reduced cardiac vagal activity after 4 wk of the onset of 1K1C hypertension (4). It has also been demonstrated that the baroreflex gain was reduced 1 day after clipping, while the major baroreflex impairment occurred after 30 days (30). A number of studies...

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Section: Discussionmentioning

confidence: 99%

Changes in hemodynamic and neurohumoral control cause cardiac damage in one-kidney, one-clip hypertensive mice

Borges

Salgado

Silva³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Arterial pressure was measured continuously via the telemetry catheter at 1,000 Hz, and sBRS was determined post hoc using the sequence method (Hemolab, Iowa City, IA) (4,52). From the arterial waveform, the software application identified ramps of heart beats in which systolic blood pressure and pulse interval both either increased or decreased.…”

Section: Determination Of Baroreflex Functionmentioning

confidence: 99%

Baroreflex sensitivity varies during the rat estrous cycle: role of gonadal steroids

Goldman¹,

Azar²,

Mulvaney³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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-Baroreflex sensitivity (BRS) increases in women during the luteal phase of the menstrual cycle, when gonadal hormones are elevated, but whether a similar cycle-dependent variation in BRS occurs in rats is unknown. In addition, whether cyclic BRS changes depend on gonadal steroids has not been previously investigated. To test these hypotheses, BRS was determined in cycling female rats using two approaches: 1) baroreflex control of renal sympathetic nerve activity (RSNA) in anesthetized rats; 2) cardiovagal spontaneous BRS (sBRS) in conscious rats instrumented for continuous telemetric measurements of mean arterial pressure (MAP) and heart rate (HR). MAP, HR, and sBRS were also measured in rats 2-3 and 5-6 wk following ovariectomy (OVX), to eliminate gonadal steroids. In anesthetized rats, RSNA BRS gain was increased (P Ͻ 0.01) during proestrus (Ϫ4.8Ϯ0.5% control/mmHg) compared with diestrus/estrus (Ϫ2.8 Ϯ 0.3% control/mmHg). Similarly, a proestrous peak in sBRS was observed in conscious rats (1.66 Ϯ 0.07 ms/mmHg, proestrus; 1.48 Ϯ 0.06 ms/mmHg, diestrus/ estrus; P Ͻ 0.001). OVX eliminated estrous cycle-induced variation in sBRS. In addition, OVX reduced (P Ͻ 0.05) diurnal variations in MAP (5.9 Ϯ 0.3 vs. 3.9 Ϯ 0.5 mmHg) and HR [54 Ϯ 4 vs. 39 Ϯ 3 beats per minute (bpm)], and abolished diurnal variations in sBRS. Finally, while MAP, HR, and sBRS were decreased 2-3 wk following OVX, ϳ3 wk later, MAP and sBRS increased, and HR decreased further. No changes in MAP, HR, or sBRS were seen with time in sham OVX controls. In summary, RSNA and cardiovagal sBRS vary during the rat estrous cycle, and this variation is abolished by OVX. We conclude that sex steroid hormones are required for both cyclic and diurnal changes in BRS in rats.renal sympathetic nerve activity; ovariectomy; diurnal; telemetry CONSIDERABLE EVIDENCE INDICATES that gonadal steroids can influence mean arterial pressure (MAP), heart rate (HR), and baroreflex sensitivity (BRS). First, sex differences have been documented (1,2,5,16,20,27). Second, MAP and HR vary during the estrous cycle of the rat (53), and, in humans, sympathetic BRS increases during the midluteal phase, when gonadal steroid hormone concentrations are higher, compared with the early follicular phase of the menstrual cycle (32). Nevertheless, whether BRS changes during the rat estrous cycle has not been studied. Moreover, whether changes in gonadal steroids underlie the reproductive cycle variability in MAP, HR, and BRS is unclear. Ovariectomy (OVX) and administration of estrogen and/or progesterone have been shown to alter MAP and HR in women and experimental animals; however, results have been conflicting (12,19,31,36,42,53,58). Furthermore, estrogen increases BRS (25,34,40,47); in contrast, a neurosteroid metabolite of progesterone, allopregnanolone, decreases BRS (18). Thus, a clear understanding of the influence of cyclic changes in endogenous gonadal steroids on MAP, HR, and BRS is lacking.Therefore, the primary goal of this study was to determine if BRS varies during the rat estrou...

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“…From baseline recordings, spontaneous baroreceptor reflex sensitivity (SBRS) was calculated using the sequence method as described. 16 …”

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confidence: 99%

Angiotensin-Converting Enzyme 2 Overexpression in the Subfornical Organ Prevents the Angiotensin II–Mediated Pressor and Drinking Responses and Is Associated With Angiotensin II Type 1 Receptor Downregulation

Feng

Yue

Xia

et al. 2008

Circulation Research

129

109

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Abstract-We recently reported the presence of angiotensin-converting enzyme (ACE)2 in brain regions controlling cardiovascular function; however, the role of ACE2 in blood pressure regulation remains unclear because of the lack of specific tools to investigate its function. We hypothesized that ACE2 could play a pivotal role in the central regulation of cardiovascular function by regulating other renin-angiotensin system components. To test this hypothesis, we generated an adenovirus expressing the human ACE2 cDNA upstream of an enhanced green fluorescent protein (eGFP) reporter gene . In vitro characterization shows that neuronal cells infected with Ad-hACE2-eGFP (10 to 100 multiplicities of infection), but not Ad-eGFP (100 multiplicities of infection), exhibit dose-dependent ACE2 expression and activity. In addition, an active secreted form was detected in the conditioned medium. In vivo, Ad-hACE2-eGFP infection (2ϫ10 6 plaque-forming units intracerebroventricularly) produced time-dependent expression and activity (with a peak at 7 days) in the mouse subfornical organ. More importantly, 7 days after virus infection, the pressor response to angiotensin (Ang) II (200 pmol intracerebroventricularly) was significantly reduced in Ad-hACE2-eGFP-treated mice compared with controls. Furthermore, subfornical organ-targeted ACE2 overexpression dramatically reduced the Ang II-mediated drinking response. Interestingly, ACE2 overexpression was associated with downregulation of the Ang II type 1 receptor expression both in vitro and in vivo. These data suggest that ACE2 overexpression in the subfornical organ impairs Ang II-mediated pressor and drinking responses at least by inhibiting the Ang II type 1 receptor expression. Taken together, our results show that ACE2 plays a pivotal role in the central regulation of blood pressure and volume homeostasis, offering a new target for the treatment of hypertension and other cardiovascular diseases. (Circ Res. 2008;102:729-736.) Key Words: adenovirus Ⅲ carboxypeptidase Ⅲ brain Ⅲ blood pressure Ⅲ gene therapy T he renin-angiotensin system (RAS) is well known for its effects on the cardiovascular system and fluid homeostasis. Classically, these effects were thought to result primarily from the systemic production of angiotensin (Ang) II. 1 Circulating Ang II stimulates Ang II type 1 (AT 1 ) receptors present in the kidney and the vasculature to produce vasoconstriction but also water and salt reabsorption. Although kidneys and liver are the major endocrine sites of renin and angiotensinogen synthesis, respectively, this view of the RAS has been challenged in the last decade because both genes have been detected in extrarenal and extrahepatic tissues. 2,3 For instance, it has become clear that a local RAS is present in several tissues, for example, the heart, adipose, vasculature, and bone marrow, with similar effects to the endocrine RAS but also more specific functions depending on the individual system. 1 One of these local systems, the brain RAS, has long been considered pivo...

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Baroreceptor Reflex Sensitivity Estimated by the Sequence Technique is Reliable in Rats

Cited by 56 publications

References 8 publications

Changes in hemodynamic and neurohumoral control cause cardiac damage in one-kidney, one-clip hypertensive mice

Changes in hemodynamic and neurohumoral control cause cardiac damage in one-kidney, one-clip hypertensive mice

Baroreflex sensitivity varies during the rat estrous cycle: role of gonadal steroids

Angiotensin-Converting Enzyme 2 Overexpression in the Subfornical Organ Prevents the Angiotensin II–Mediated Pressor and Drinking Responses and Is Associated With Angiotensin II Type 1 Receptor Downregulation

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