Age- and Sex-Related Changes in Heart Rate Variability Under Conditions of Blockade or Stimulation of Peripheral Adrenoceptor in Outbred Rats

Abstract

Changes in heart rhythm variability were studied in male and female mature and 5-6-week-old rats under conditions of 7-day administration of β1-adrenoreceptor blocker atenolol (2.5 mg/kg) and α1-adrenoreceptor agonist phenylephrine (0.3 mg/kg). Atenolol administration to mature rats was followed by a slight deceleration of cardiac rhythm, a tendency to heart rate variability decrease in the HF range, and moderate increase in centralization of regulation. In 6-week-old rats, increased variability of cardiointervals and significant increase of centralization of the heart rhythm regulation due to an increase in the power of low-frequency waves (specifically VLF) were observed. In both mature and young rats, changes of heart rate frequency and variability in response to atenolol administration were more pronounced in females. Phenylephrine administration was followed by a significant heart rate deceleration, increase in cardiointerval variability and centralization of heart rate regulation in mature rats and by a decrease in heart rate variability in all frequency ranges in 6-week-old rats. In mature rats, changes in heart rate frequency and variability produced by phenylephrine administration were more pronounced in males; in young rats, the most strained heart rhythm developed in females.

Cardiac autonomic modulation induced by doxorubicin in a rodent model of colorectal cancer and the influence of fullerenol pretreatment

“…However, there are several studies demonstrating the impact of different autonomic and non-autonomic factors on HRV, which could be associated with DOX-induced cardiotoxicity. Concerning autonomic factors, modulation of autonomic nervous activity to the heart, adrenoceptor (AR) and muscarinic receptor density [59, 60], their function [46] and AR receptor activated intracellular signaling pathways [46,61] are proposed while suggested non-autonomic factors mainly include inflammation [62,63] and oxidative stress [46,63,64]. Based on the reports of the above-mentioned studies, some potential mechanisms underlying the HRV modulation in DOX-induced cardiotoxicity observed in the present research might be proposed.…”

An Integrative Literature Review of Heart Rate Variability Measures to Determine Autonomic Nervous System Responsiveness Using Pharmacological Manipulation

“…The 19 studies listed in Table 2 met the review criteria, and quality appraisal of these studies is outlined in Supplemental Digital Content 3, Supplemental Table S3, http://links.lww.com/JCN/A212. Of these manuscripts, 11 were human HRV studies [17][18][19][20][21][22][23][24][25][26][27] and 8 were preclinical rodent HRV studies [28][29][30][31][32][33][34][35] (Table 2). In 18 of the studies, data on adult humans or animals were reported, whereas data on children (median age, 10 years) were reported in 1 study.…”

“…In preclinical rodent studies that used b-adrenergic receptors blocking medication (ie, propranolol, atenolol, and metoprolol), pharmacologic SNS blockade was associated with an increase in the mean normal-normal interval (milliseconds) in most studies, 28,[30][31][32]34,35 with the exception of Silva et al, 33 who reported no normalnormal interval change, and Kur'yanova et al, 29 who only reported a change in female rats. In addition, the standard deviation of normal-normal intervals (SDNN) decreased in the 3 animal studies using b-adrenergic receptor blockers who reported this metric.…”

“…A total of 14 studies evaluated HRV response to sympathetic blockade using propranolol and clonidine in human studies, 18,19 and propranolol, DL-propranolol hydrochloride, atenolol, metoprolol, phentolamine, and prazosin in preclinical rodent studies. [29][30][31]33,34 Propranolol and atenolol were the primary medications used to block effects of the SNS by binding to badrenergic receptors, whereas phentolamine, clonidine, and prazosin were used to block ɑ1-adrenergic receptors (Table 2; see Supplemental Digital Content 1, Supplemental Table S1, http://links.lww.com/JCN/A210, for medication routes and dosages).…”

Effect of anaesthetic and choice of neuromuscular blocker on vagal control of heart rate under laboratory animal experimental conditions

“…10 Nevertheless, administration of atenolol has been shown to alter HF power with variable responses observed that appear to be age-, sex- or disease-dependent or relate to the duration of atenolol administration. 16–19 The exact mechanism by which atenolol changes HF power remains unclear, but may relate to the sympathovagal interactions that are present at the level of the sinoatrial (SA) node. MAP and SBPV were unchanged by atenolol, indicating appropriate compensatory neurohormonal mechanisms were subsequently able to maintain normal BP in the face of a decrease in HR and loss of any β 1 -adrenoceptor-mediated vasodilatory actions.…”