Biomedical subjects

Dwayne N Jackson

Publications and source records attributed to Dwayne N Jackson.

5 recordsLinked to original sources

PubMed2005

Neuropeptide Y bioavailability is suppressed in the hindlimb of female Sprague-Dawley rats.

We recently reported that male, but not female, rats exhibit basal endogenous neuropeptide Y Y(1)-receptor modulation of hindlimb vasculature. The lack of baseline endo-genous Y(1)-receptor control in females was evident despite the expression of Y(1)-receptors and neuropeptide Y in hindlimb skeletal muscle tissue. The following study addressed the hypothesis that neuropeptide Y bioavailability is blunted in female rats under baseline conditions. It was further hypothesized that enhanced prejunctional autoinhibitory neuropeptide Y Y(2)-receptor expression and/or proteolytic processing of released neuropeptide Y may persist in female rats. Using western blot analysis, it was observed that females had greater overall neuropeptide Y Y(2)-receptor expression in skeletal muscle compared to males (P < 0.05). To address the prevalence/impact of baseline endogenous Y(2)-receptor activation on neuropeptide Y release in hindlimb vasculature, an arterial infusion of BIIE0246 (specific non-peptide Y(2)-receptor antagonist; 170 microg kg(-1)) was carried out on female and male rats. Y(2)-receptor blockade resulted in a decrease in hindlimb vascular conductance in females and males (P < 0.05). However, the BIIE0246-induced decrease in vascular conductance was Y(1)-receptor dependent in females, but not males (P < 0.05). In addition, compared to baseline, BIIE0246 infusion resulted in increased plasma neuropeptide Y concentration in females (P < 0.05), while there was no observable change in males. In a final experiment, systemic inhibition of proteolytic enzymes dipeptidylpeptidase IV (via 500 nM diprotin A) and aminopeptidase P (via 180 nM 2-mercaptoethanol) elicited a Y(1)-receptor-dependent decrease in hindlimb vascular conductance in females (P < 0.05). It was concluded that our previously reported lack of basal endogenous Y(1)-receptor activation in female hindlimb vasculature was (at least partially) due to prejunctional Y(2)-receptor autoinhibition and proteolytic processing of neuropeptide Y.

Aminopeptidases↗

PubMed2004

Gender-modulated endogenous baseline neuropeptide Y Y1-receptor activation in the hindlimb of Sprague-Dawley rats.

This study examined the effect of neuropeptide Y Y(1)-receptor blockade both alone, and in interaction with alpha(1)-adrenoceptor antagonism, on basal hindlimb vascular conductance in male and female Sprague-Dawley rats. Hindlimb vascular conductance was measured during infusion of BIBP3226 (Y(1)-receptor antagonist; 100 microg kg(-1)), prazosin (alpha(1)-receptor antagonist; 20 microg kg(-1)), and combined blockade. In males, vascular conductance increased 1.1 +/- 0.3 microl min(-1) mmHg(-1) above baseline with BIBP3226, and 2.4 +/- 0.4 microl min(-1) mmHg(-1) above baseline with prazosin (both P < 0.05). The increase in vascular conductance during combined blockade (5.1 +/- 0.7 microl min(-1) mmHg(-1)) was greater than the sum of the independent BIBP3226 and prazosin responses (P < 0.05). In females, basal hindlimb vascular conductance was unaffected by Y(1)-receptor blockade. However, alpha(1)-receptor blockade resulted in a 3.5 +/- 0.6 microl min(-1) mmHg(-1) increase in vascular conductance above baseline, which was not different than the combined blockade condition. Males had greater skeletal muscle neuropeptide Y concentration (P < 0.05; ELISA) than females. Furthermore, compared with females, male skeletal muscle contained greater Y(1)-receptor expression (P < 0.05; Western blot). It was concluded that, under baseline conditions, agonist and receptor-based mechanisms for Y(1)-receptor dependent control of vascular conductance in skeletal muscle was greater in male versus female rats.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed2004

Y1- and alpha1-receptor control of basal hindlimb vascular tone.

The role of endogenous Y(1)-receptor activation on skeletal muscle vasculature under baseline conditions is currently debated and no in vivo studies have been performed to address this issue. Therefore, this study was designed to address the effect of Y(1)-receptor and/or alpha(1)-adrenoceptor antagonism on basal hindlimb vascular conductance in male Sprague-Dawley rats in vivo. Left hindlimb vascular conductance, carotid artery mean arterial pressure, and heart rate were measured during low volume infusion of N(2)-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]-d-arginine amide (BIBP3226; 100 microg/kg), prazosin (20 microg/kg), and combined blockade to the left hindlimb. Vascular conductance increased 1.5 +/- 0.5 microl.min(-1).mmHg(-1) with BIBP3226 infusion, 1.7 +/- 0.5 microl.min(-1).mmHg(-1) with prazosin infusion, and 4.8 +/- 1.0 microl.min(-1).mmHg(-1) with combined blockade (P < 0.05). Interestingly, systolic vascular conductance increased in all three conditions, but diastolic vascular conductance only increased in the two conditions where BIBP3226 was present. These data indicate that Y(1)-receptor activation plays an important role in the regulation of vascular conductance in the resting rat hindlimb. Furthermore, this effect was of the same magnitude as the alpha(1)-adrenoceptor contribution. The differential flow profiles following alpha(1) blockade with and without Y(1)-receptor blockade supports local differences in receptor distribution.

Adrenergic alpha-Antagonists↗

PubMed2003

Change in spontaneous baroreflex control of pulse interval during heat stress in humans.

Spontaneous baroreflex control of pulse interval (PI) was assessed in healthy volunteers under thermoneutral and heat stress conditions. Subjects rested in the supine position with their lower legs in a water bath at 34 degrees C. Heat stress was imposed by increasing the bath temperature to 44 degrees C. Arterial blood pressure (Finapres), PI (ECG), esophageal and skin temperature, and stroke volume were continuously collected during each 5-min experimental stage. Spontaneous baroreflex function was evaluated by multiple techniques, including 1) the mean slope of the linear relationship between PI and systolic blood pressure (SBP) with three or more simultaneous increasing or decreasing sequences, 2) the linear relationship between changes in PI and SBP (deltaPI/DeltaSBP) derived by using the first differential equation, 3) the linear relationship between changes in PI and SBP with simultaneously increasing or decreasing sequences (+deltaPI/+deltaSBP or -deltaPI/-deltaSBP), and 4) transfer function analysis. Heat stress increased esophageal temperature by 0.6 +/- 0.1 degrees C, decreased PI from 1,007 +/- 43 to 776 +/- 37 ms and stroke volume by 16 +/- 5 ml/beat. Heat stress reduced baroreflex sensitivity but increased the incidence of baroreflex slopes from 5.2 +/- 0.8 to 8.6 +/- 0.9 sequences per 100 heartbeats. Baroreflex sensitivity was significantly correlated with PI or vagal power (r2 = 0.45, r2 = 0.71, respectively; P < 0.05). However, the attenuation in baroreflex sensitivity during heat stress appeared related to a shift in autonomic balance (shift in resting PI) rather than heat stress per se.

Adult↗

PubMed2003

Upright LBPP application attenuates elevated postexercise resting thresholds for cutaneous vasodilation and sweating.

We evaluated postexercise venous pooling as a factor leading to previously reported increases in the postexercise esophageal temperature threshold for cutaneous vasodilation (ThVD) and sweating (ThSW). Six subjects were randomly exposed to lower body positive pressure (LBPP) and to no LBPP after an exercise and no-exercise treatment protocol. The exercise treatment consisted of 15 min of upright cycling at 65% of peak oxygen consumption, and the no-exercise treatment consisted of 15 min upright seated rest. Immediately after either treatment, subjects donned a liquid-conditioned suit used to regulate mean skin temperature and then were positioned within an upright LBPP chamber. The suit was first perfused with 20 degrees C water to control and stabilize skin and core temperature before whole body heating. Subsequently the skin was heated ( approximately 4.0 degrees C/h) until cutaneous vasodilation and sweating occurred. Forearm skin blood flow and arterial blood pressure were measured noninvasively and were used to calculate cutaneous vascular conductance during whole body heating. Sweat rate response was estimated from a 5.0-cm2 ventilated capsule placed on the upper back. Postexercise ThVD and ThSW were both significantly elevated (0.27 +/- 0.04 degrees C and 0.25 +/- 0.04 degrees C, respectively) compared with the no-exercise trial without LBPP (P < 0.05). However, the postexercise increases in both ThVD and ThSW were reversed with the application of LBPP. Our results support the hypothesis that the postexercise warm thermal responses of cutaneous vasodilation and sweating are attenuated by baroreceptor modulation via lower body venous pooling.

Adult↗