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Baroreflex responses to electrical stimulation of aortic depressor nerve in conscious SHR.
. 2007 Jan; 292(1):H593-600.

Abstract

Baroreflex responses to changes in arterial pressure are impaired in spontaneously hypertensive rats (SHR). Mean arterial pressure (MAP), heart rate (HR), and regional vascular resistances were measured before and during electrical stimulation (5-90 Hz) of the left aortic depressor nerve (ADN) in conscious SHR and normotensive control rats (NCR). The protocol was repeated after beta-adrenergic-receptor blockade with atenolol. SHR exhibited higher basal MAP (150 +/- 5 vs. 103 +/- 2 mmHg) and HR (393 +/- 9 vs. 360 +/- 5 beats/min). The frequency-dependent hypotensive response to ADN stimulation was preserved or enhanced in SHR. The greater absolute fall in MAP at higher frequencies (-68 +/- 5 vs. -38 +/- 3 mmHg at 90-Hz stimulation) in SHR was associated with a preferential decrease in hindquarter (-43 +/- 5%) vs. mesenteric (-27 +/- 3%) resistance. In contrast, ADN stimulation decreased hindquarter and mesenteric resistances equivalently in NCR (-33 +/- 7% and -30 +/- 7%). Reflex bradycardia was also preserved in SHR, although its mechanism differed. Atenolol attenuated the bradycardia in SHR (-88 +/- 14 vs. -129 +/- 18 beats/min at 90-Hz stimulation) but did not alter the bradycardia in NCR (-116 +/- 16 vs. -133 +/- 13 beats/min). The residual bradycardia under atenolol (parasympathetic component) was reduced in SHR. MAP and HR responses to ADN stimulation were also preserved or enhanced in SHR vs. NCR after deafferentation of carotid sinuses and contralateral right ADN. The results demonstrate distinct differences in central baroreflex control in conscious SHR vs. NCR. Inhibition of cardiac sympathetic tone maintains reflex bradycardia during ADN stimulation in SHR despite impaired parasympathetic activation, and depressor responses to ADN stimulation are equivalent or even greater in SHR due to augmented hindquarter vasodilation.

Authors+Show Affiliations

Dept. of Physiology, School of Medicine of Ribeirão Preto, Univ. of São Paulo, Av. Bandeirantes, 3900, 14049-900 Ribeirão Preto, SP, Brazil. hcsalgad@fmrp.usp.brNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16951050

Citation

Salgado, Helio C., et al. "Baroreflex Responses to Electrical Stimulation of Aortic Depressor Nerve in Conscious SHR." American Journal of Physiology. Heart and Circulatory Physiology, vol. 292, no. 1, 2007, pp. H593-600.
Salgado HC, Barale AR, Castania JA, et al. Baroreflex responses to electrical stimulation of aortic depressor nerve in conscious SHR. Am J Physiol Heart Circ Physiol. 2007;292(1):H593-600.
Salgado, H. C., Barale, A. R., Castania, J. A., Machado, B. H., Chapleau, M. W., & Fazan, R. (2007). Baroreflex responses to electrical stimulation of aortic depressor nerve in conscious SHR. American Journal of Physiology. Heart and Circulatory Physiology, 292(1), H593-600.
Salgado HC, et al. Baroreflex Responses to Electrical Stimulation of Aortic Depressor Nerve in Conscious SHR. Am J Physiol Heart Circ Physiol. 2007;292(1):H593-600. PubMed PMID: 16951050.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Baroreflex responses to electrical stimulation of aortic depressor nerve in conscious SHR. AU - Salgado,Helio C, AU - Barale,Alvaro R, AU - Castania,Jaci A, AU - Machado,Benedito H, AU - Chapleau,Mark W, AU - Fazan,Rubens,Jr Y1 - 2006/09/01/ PY - 2006/9/5/pubmed PY - 2007/2/21/medline PY - 2006/9/5/entrez SP - H593 EP - 600 JF - American journal of physiology. Heart and circulatory physiology JO - Am. J. Physiol. Heart Circ. Physiol. VL - 292 IS - 1 N2 - Baroreflex responses to changes in arterial pressure are impaired in spontaneously hypertensive rats (SHR). Mean arterial pressure (MAP), heart rate (HR), and regional vascular resistances were measured before and during electrical stimulation (5-90 Hz) of the left aortic depressor nerve (ADN) in conscious SHR and normotensive control rats (NCR). The protocol was repeated after beta-adrenergic-receptor blockade with atenolol. SHR exhibited higher basal MAP (150 +/- 5 vs. 103 +/- 2 mmHg) and HR (393 +/- 9 vs. 360 +/- 5 beats/min). The frequency-dependent hypotensive response to ADN stimulation was preserved or enhanced in SHR. The greater absolute fall in MAP at higher frequencies (-68 +/- 5 vs. -38 +/- 3 mmHg at 90-Hz stimulation) in SHR was associated with a preferential decrease in hindquarter (-43 +/- 5%) vs. mesenteric (-27 +/- 3%) resistance. In contrast, ADN stimulation decreased hindquarter and mesenteric resistances equivalently in NCR (-33 +/- 7% and -30 +/- 7%). Reflex bradycardia was also preserved in SHR, although its mechanism differed. Atenolol attenuated the bradycardia in SHR (-88 +/- 14 vs. -129 +/- 18 beats/min at 90-Hz stimulation) but did not alter the bradycardia in NCR (-116 +/- 16 vs. -133 +/- 13 beats/min). The residual bradycardia under atenolol (parasympathetic component) was reduced in SHR. MAP and HR responses to ADN stimulation were also preserved or enhanced in SHR vs. NCR after deafferentation of carotid sinuses and contralateral right ADN. The results demonstrate distinct differences in central baroreflex control in conscious SHR vs. NCR. Inhibition of cardiac sympathetic tone maintains reflex bradycardia during ADN stimulation in SHR despite impaired parasympathetic activation, and depressor responses to ADN stimulation are equivalent or even greater in SHR due to augmented hindquarter vasodilation. SN - 0363-6135 UR - https://www.unboundmedicine.com/medline/citation/16951050/Baroreflex_responses_to_electrical_stimulation_of_aortic_depressor_nerve_in_conscious_SHR_ L2 - https://journals.physiology.org/doi/10.1152/ajpheart.00181.2006?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -