Sexual dimorphism in prostanoid-potentiated vascular contraction: roles of endothelium and ovarian steroids.
*Sex Characteristics; Animals; Aorta/drug effects/physiology; Bridged Bicyclo Compounds; Cyclooxygenase Inhibitors/pharmacology; Endothelium; Enzyme Inhibitors/pharmacology; Estrogens/*physiology; Fatty Acids; Female; Heterocyclic; Hydrazines/pharmacology; Imidazoles/pharmacology; Indomethacin/pharmacology; Male; Ovariectomy; Phenylephrine/pharmacology; Progesterone/*physiology; Prostaglandins/*metabolism; Rats; Sprague-Dawley; Thromboxanes/metabolism; Unsaturated; Vascular/*metabolism; Vasoconstriction/drug effects/*physiology; Vasoconstrictor Agents/pharmacology; Vasopressins/pharmacology
The effects of constrictor prostanoid (CP) pathway inhibitors on vascular reactivity to vasopressin (VP) and phenylephrine (PE) were examined in thoracic aortas of male, female, and ovariectomized (OVX) female Sprague-Dawley rats. Maximal contractile response of control (Cont) aortas to VP was markedly higher in females (3,885 +/- 332 mg/mg ring wt) than in males (810 +/- 148 mg). Indomethacin (Indo; 10 microM) attenuated maximal response to VP in females (3,043 +/- 277 mg) but not in males. SQ-29,548 (SQ; 1 microM) attenuated maximal response to VP in females (3,042 +/- 290 mg) to a similar extent as Indo. Dazoxiben (Daz; 10 microM) alone had no effect, but Daz + SQ attenuated maximal contractile response to VP to a similar extent as SQ alone. Removal of the endothelium in female aortas attenuated contractile responses to VP in Cont aortas. OVX attenuated maximal contractile response to VP in Cont aortas (2,093 +/- 329 mg) and abolished the attenuating effects of Indo. Indo, SQ, and Daz exerted identical effects on contractile responses of male, female, and OVX female aortas to PE. These findings establish the following in the rat aorta: 1) CP, probably thromboxane and/or endoperoxide, is responsible for approximately
Fulton Clifford T; Stallone John N
American journal of physiology. Heart and circulatory physiology
2002
2002-11
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/ajpheart.00099.2002" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00099.2002</a>
Local modulation of adrenergic responses in the hindlimb vasculature of the intact conscious rat.
Adrenergic Agonists/*pharmacology; Animals; Arginine/analogs & derivatives/pharmacology; Cyclooxygenase Inhibitors/pharmacology; Female; Hemodynamics/*drug effects/physiology; Hindlimb/*blood supply/drug effects/metabolism; Indomethacin/pharmacology; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide Synthase/antagonists & inhibitors; Rats; Sprague-Dawley
1. Local modulation of adrenergic responses was examined in the hindlimb vasculature of chronically instrumented intact conscious rats. Sprague-Dawley rats (n = 22) were instrumented with a Doppler flow probe around the right common iliac artery, a polyethylene catheter inserted just distal to the flow probe and a left carotid arterial catheter. 2. The effects of various concentrations of the alpha 1-adrenergic receptor agonist phenylephrine (0.005-0.075 microgram kg-1), the alpha 2-adrenergic receptor agonist clonidine (0.1-0.7 microgram kg-1), and the endogenous adrenergic receptor agonist adrenaline (0.02-0.08 microgram kg-1), were investigated under control conditions, and in the presence of the nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine methyl ester hydrochoride (L-NAME) (NO-X, 0.2 mg kg-1) and the cyclo-oxygenase inhibitor indomethacin (CO-X, 10 mg kg-1). Results were presented as dose-response curves. 3. Heart rate and arterial pressure were not altered by any of the agents because all were locally injected into the hindlimb vasculature and the selected doses were lower than those which elicited systemic responses. 4. Maximal vasoconstrictor responses to phenylephrine were enhanced in the presence of NO-X (50 +/- 6%) and
DiCarlo S E; Patil R D; Collins H L; Chen C Y
The Journal of physiology
1995
1995-06
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1113/jphysiol.1995.sp020771" target="_blank" rel="noreferrer noopener">10.1113/jphysiol.1995.sp020771</a>