Systemic arterial pressor responses induced by potassium in dogfish, Squalus acanthias

1981 ◽  
Vol 241 (3) ◽  
pp. R228-R232
Author(s):  
D. F. Opdyke ◽  
R. G. Carroll ◽  
N. E. Keller
Keyword(s):  
Pressor Response ◽  
Muscle Tension ◽  
Plasma Catecholamines ◽  
Blocking Agent ◽  
Adrenergic Stimulation ◽  
Direct Exposure ◽  
Pressor Responses ◽  
Before And After ◽  
K Concentration

Intravascular injection of small doses of potassium (0.025-0.5 meq) into dogfish results in dose-related dorsal aortic pressor responses. The responses are blocked by phentolamine, an alpha-adrenergic blocking agent. Assays of plasma catecholamines before and after injection of potassium (K+) showed that plasma levels of epinephrine (E) and norepinephrine (NE) had increased significantly (E, 314%; NE, 233%) 1 min after injection. The pressor responses were initiated 40-90 s after K+ injection at which time plasma E and NE levels were already significantly elevated. Experiments on isolated dogfish arterial strips showed that phentolamine cannot block the increase in vascular smooth muscle tension that occurs after direct exposure to small increases (0.003 meq/ml) in K+ concentration. Because phentolamine effectively blocks the pressor response to even higher doses of K+ in vivo, it is thought that, in addition to any direct vasoconstrictor effect or K+, the adrenergic stimulation provided by catecholamine release is required to produce the observed pressor response.

In vivo evidence for endothelin-1-mediated attenuation of α1-adrenergic stimulation

2006 ◽  
Vol 290 (3) ◽  
pp. H1251-H1258 ◽  
Author(s):  
Gerard D’Angelo ◽  
Jennifer S. Pollock ◽  
David M. Pollock
Keyword(s):  
Acute Stress ◽  
Pressor Response ◽  
Area Under The Curve ◽  
Receptor Activation ◽  
Plasma Norepinephrine ◽  
Adrenergic Stimulation ◽  
Endothelin 1 ◽  
Air Jet ◽  
Before And After

Experiments were designed to determine the influence of endothelin A (ETA) receptors on the pressor response to acute environmental stress in Dahl salt-resistant (DR) and Dahl-sensitive (DS) rats. Mean arterial pressure (MAP) was chronically monitored by telemetry before and after treatment with the selective ETA receptor antagonist ABT-627. Rats were restrained and subjected to pulsatile air jet stress (3 min). In untreated animals, the total pressor response (area under the curve) to acute stress was not different between DR vs. DS rats (8.1 ± 1.7 vs. 15.6 ± 2.6 mmHg × 3 min, P = 0.10). Conversely, treatment with ABT-627 potentiated the total pressor response only in DR rats (36.3 ± 6.2 vs. 22.6 ± 5.9 mmHg × 3 min, DR vs. DS, P < 0.05). Treatment with ABT-627 allowed greater responses in anesthetized DR rats to exogenous phenylephrine (1–4 μg/kg) during ganglionic blockade ( P < 0.05) and produced a significant increase in plasma norepinephrine at baseline and during stress in conscious DR rats compared with untreated animals ( P < 0.05). ETA receptor blockade had no effect on these responses in DS rats. Our results suggest that endothelin-1 can inhibit α-adrenergic-mediated effects in DR, but not DS rats, consistent with the hypothesis that ETA receptor activation functions to reduce sympathetic nerve activity and responses in vascular smooth muscle to sympathetic stimulation.

Inotropic sensitivity to beta-adrenergic stimulation in early sepsis

1988 ◽  
Vol 255 (4) ◽  
pp. H699-H703 ◽  
Author(s):  
L. W. Smith ◽  
K. H. McDonough
Keyword(s):  
Contractile Function ◽  
Plasma Catecholamines ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Maximal Increase ◽  
Beta Adrenergic ◽  
Arterial Blood ◽  
Myocardial Contractile ◽  
Early Sepsis

In early sepsis, maintenance of in vivo cardiovascular performance is at least partly dependent on sympathetic support to hearts with intrinsic contractile defects. Yet prolonged sympathetic stimulation, as occurs in sepsis, would be expected to alter the heart's ability to respond to this stimulation. We have investigated myocardial inotropic sensitivity to beta-adrenergic stimulation in a model of sepsis in which animals, at the time studied, exhibited bacteremia, normal arterial blood pressure and cardiac output, elevated heart rate, and elevated plasma catecholamines. Intrinsic myocardial contractile function, as assessed by the maximal rate of left ventricular pressure development (LV dP/dtmax) in an isovolumically contracting heart preparation, was significantly depressed in septic animals. To determine whether hearts from septic animals could respond normally to beta-adrenergic stimulation, we studied inotropic response to a bolus of isoproterenol in these isolated hearts. With maximal isoproterenol stimulation, hearts from septic animals were able to attain the same dP/dtmax as were hearts from control animals. With lower levels of isoproterenol, there was also no difference in inotropic indexes between the two groups when response was expressed as a percent of the maximal increase in dP/dtmax achieved with isoproterenol. These results suggest that in early sepsis, despite intrinsic myocardial contractile dysfunction, the ability of the heart to modulate its inotropic state in response in beta-adrenergic stimulation is intact.

Baroreflex attenuates pressor response to graded muscle ischemia in exercising dogs

1990 ◽  
Vol 258 (2) ◽  
pp. H305-H310 ◽  
Author(s):  
D. D. Sheriff ◽  
D. S. O'Leary ◽  
A. M. Scher ◽  
L. B. Rowell
Keyword(s):  
Perfusion Pressure ◽  
Pressor Response ◽  
Vascular Occlusion ◽  
Arterial Baroreceptors ◽  
Systemic Pressure ◽  
Muscle Ischemia ◽  
Pressor Responses ◽  
Before And After ◽  
Muscle Chemoreflex ◽  
Arterial Baroreceptor

Graded reductions in hindlimb perfusion in dogs exercising at 2 miles/h (0% grade) elicited reflex pressor responses by what is referred to as the “muscle chemoreflex.” To determine the extent to which arterial baroreceptor reflexes oppose the muscle chemoreflex, we elicited pressor responses to muscle ischemia before and after chronic surgical denervation of the arterial baroreceptors. The muscle chemoreflex showed a threshold beyond which systemic pressure rose approximately 3 mmHg for each 1-mmHg decrease in hindlimb perfusion pressure when the arterial baroreceptors were intact. Arterial baroreceptor denervation approximately doubled the pressor responses, i.e., systemic pressure rose by approximately 6 mmHg for each 1-mmHg fall in hindlimb perfusion pressure, without alteration in threshold. We conclude that during mild dynamic exercise, the arterial baroreflexes oppose the pressor response to graded reductions in hindlimb perfusion, reducing it by approximately 50%. When unopposed by the arterial baroreflexes the muscle chemoreflex exhibits a gain (ratio of change in systemic pressure to change in hindlimb perfusion pressure) of approximately -6; thus this reflex can correct by 85% the decrease in muscle perfusion pressure caused by partial vascular occlusion.

Prostaglandin synthetase inhibitors do not decrease hypoxic pulmonary vasoconstriction

1976 ◽  
Vol 41 (5) ◽  
pp. 714-718 ◽  
Author(s):  
E. K. Weir ◽  
I. F. McMurtry ◽  
A. Tucker ◽  
J. T. Reeves ◽  
R. F. Grover
Keyword(s):  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Prostaglandin Synthesis ◽  
Pulmonary Vasoconstriction ◽  
Pressor Responses ◽  
Hypoxic Vasoconstriction ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Prostaglandin Antagonists ◽  
The Stability

Prostaglandins are naturally occurring substances with powerful vasoactive effects that are released from tissues during hypoxia or ischemia. Several workers have suggested that a prostaglandin may help to mediate the pulmonary vascular pressor response to alveolar hypoxia. To investigate this possibility, we have measured the pressor responses to hypoxia before and after prostaglandin synthesis antagonism with meclofenamate in eight anesthetized dogs, two groups of awake calves (n=10 and =5), and nine isolated, perfused rat lungs. In addition, synthesis was inhibited by the use of indomethacin in nine additional dogs. The stability of the pulmonary vascular response to repeated hypoxic challenges was demonstrated in nine other dogs. In each species and with both prostaglandin antagonists, the pulmonary pressorresponses to hypoxia were significantly increased rather than reduced. We conclude that prostaglandins do not mediate the pulmonary vasoconstriction caused by hypoxia. The consistent increase observed suggests that hypoxic vasoconstriction stimulates prostaglandin synthesis, the net effect of which is pulmonary vasodilatation which opposes the constriction.

Baroreflex buffering of pressor response to vasopressin is mediated by V1, not V2, receptors in conscious rats

1993 ◽  
Vol 264 (2) ◽  
pp. R345-R349
Author(s):  
K. Shimizu ◽  
J. Schwartz ◽  
B. P. McGrath
Keyword(s):  
Heart Rate ◽  
Receptor Agonist ◽  
Pressor Response ◽  
Conscious Rat ◽  
Conscious Rats ◽  
Pressor Responses ◽  
Autonomic Blockade ◽  
V2 Receptor ◽  
Intact Rats

Arginine vasopressin (AVP) enhances reflex buffering of its own pressor response, thus attenuating its vasoconstrictor potential in vivo. To investigate the extent to which this effect of AVP is mediated by V1 or V2 receptors, mean arterial pressure (MAP) and heart rate (HR) changes were examined in response to graded injections of AVP or [Phe2,Orn8]oxytocin, a potent, selective V1-receptor agonist, in the absence and presence of infusion of [Val4,D-Arg8]VP, a selective V2-receptor agonist. Responses were compared in intact and autonomically blocked conscious rats. During autonomic blockade with methscopolamine and hexamethonium, the pressor sensitivities to AVP and [Phe2,Orn8]oxytocin were similarly increased. Infusion of the V2-receptor agonist had no effect by itself on MAP or HR in conscious intact rats. It also did not alter the pressor responses to the V1 agonist, in either intact or autonomically blocked rats. In the presence of the V2 agonist, the decrease in heart rate induced by the V1 agonist was enhanced. These results indicate that reflex buffering of the pressor response to AVP in the conscious rat is mediated by V1 and not V2 receptors. However, V2 receptors may be involved in modulating the heart rate response to AVP.

Liver glycogen synthase and phosphorylase changes in vivo with hypoxia and anesthetics

1982 ◽  
Vol 243 (3) ◽  
pp. E182-E187
Author(s):  
J. Theen ◽  
D. P. Gilboe ◽  
F. Q. Nuttall
Keyword(s):  
Surgical Procedure ◽  
Glycogen Phosphorylase ◽  
Glycogen Synthase ◽  
Liver Glycogen ◽  
Blocking Agent ◽  
Adrenergic Stimulation ◽  
Adrenergic Antagonists ◽  
Ganglionic Blocking

Methods for obtaining and processing rat liver for determination of glycogen phosphorylase a and synthase I activity were studied. An extremely rapid and profound increase in phosphorylase was induced by hypoxia. The effect on synthase I was slower and less striking. Using alpha- and beta-adrenergic antagonists, a catecholamine-depleting agent, and a ganglionic blocking agent, it was determined that adrenergic stimulation secondary to the surgical procedure required to obtain the liver was not a significant factor. The anesthetic agent used also had a significant effect on the proportion of phosphorylase in the a form. Seconal anesthesia resulted in lower phosphorylase a levels than did ether or urethan anesthesia.

Attenuated arterial baroreflex buffering of muscle metaboreflex in heart failure

2005 ◽  
Vol 289 (6) ◽  
pp. H2416-H2423 ◽  
Author(s):  
Jong-Kyung Kim ◽  
Javier A. Sala-Mercado ◽  
Robert L. Hammond ◽  
Jaime Rodriguez ◽  
Tadeusz J. Scislo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pressor Response ◽  
Dynamic Exercise ◽  
Arterial Baroreflex ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Before And After ◽  
Chronically Instrumented Dogs

Previous studies have shown that heart failure (HF) or sinoaortic denervation (SAD) alters the strength and mechanisms of the muscle metaboreflex during dynamic exercise. However, it is still unknown to what extent SAD may modify the muscle metaboreflex in HF. Therefore, we quantified the contribution of cardiac output (CO) and peripheral vasoconstriction to metaboreflex-mediated increases in mean arterial blood pressure (MAP) in conscious, chronically instrumented dogs before and after induction of HF in both barointact and SAD conditions during mild and moderate exercise. The muscle metaboreflex was activated via partial reductions in hindlimb blood flow. After SAD, the metaboreflex pressor responses were significantly higher with respect to the barointact condition despite lower CO responses. The pressor response was significantly lower in HF after SAD but still higher than that of HF in the barointact condition. During control experiments in the barointact condition, total vascular conductance summed from all beds except the hindlimbs did not change with muscle metaboreflex activation, whereas in the SAD condition both before and after induction of HF significant vasoconstriction occurred. We conclude that SAD substantially increased the contribution of peripheral vasoconstriction to metaboreflex-induced increases in MAP, whereas in HF SAD did not markedly alter the patterns of the reflex responses, likely reflecting that in HF the ability of the arterial baroreflex to buffer metaboreflex responses is impaired.

Arterial baroreflex alters strength and mechanisms of muscle metaboreflex during dynamic exercise

2005 ◽  
Vol 288 (3) ◽  
pp. H1374-H1380 ◽  
Author(s):  
Jong-Kyung Kim ◽  
Javier A. Sala-Mercado ◽  
Jaime Rodriguez ◽  
Tadeusz J. Scislo ◽  
Donal S. O'Leary
Keyword(s):  
Pressor Response ◽  
Dynamic Exercise ◽  
Arterial Baroreflex ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Major Mechanism ◽  
Pressor Responses ◽  
Before And After ◽  
Chronically Instrumented Dogs

Previous studies showed that the arterial baroreflex opposes the pressor response mediated by muscle metaboreflex activation during mild dynamic exercise. However, no studies have investigated the mechanisms contributing to metaboreflex-mediated pressor responses during dynamic exercise after arterial baroreceptor denervation. Therefore, we investigated the contribution of cardiac output (CO) and peripheral vasoconstriction in mediating the pressor response to graded reductions in hindlimb perfusion in conscious, chronically instrumented dogs before and after sinoaortic denervation (SAD) during mild and moderate exercise. In control experiments, the metaboreflex pressor responses were mediated via increases in CO. After SAD, the metaboreflex pressor responses were significantly greater and significantly smaller increases in CO occurred. During control experiments, nonischemic vascular conductance (NIVC) did not change with muscle metaboreflex activation, whereas after SAD NIVC significantly decreased with metaboreflex activation; thus SAD shifted the mechanisms of the muscle metaboreflex from mainly increases in CO to combined cardiac and peripheral vasoconstrictor responses. We conclude that the major mechanism by which the arterial baroreflex buffers the muscle metaboreflex is inhibition of metaboreflex-mediated peripheral vasoconstriction.

α1-Adrenoceptor Blockade: Dissociation of Its Effects on Renin Release and Arterial Blood Pressure in Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 307s-309s ◽  
Author(s):  
A. Morganti ◽  
Carla Sala ◽  
Anna Palermo ◽  
Lucia Turolo ◽  
A. Zanchetti
Keyword(s):  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Pressor Response ◽  
Plasma Renin ◽  
Test Dose ◽  
Blocking Agent ◽  
Renin Activity ◽  
Renin Release ◽  
Arterial Blood ◽  
Before And After

1. The possibility that the juxtaglomerular α1-adrenoceptors mediate an inhibitory action on renin release in man was examined in seven patients with essential hypertension, by measuring (i) the acute effects of prazosin (0.25 mg intravenously), a selective α1-adrenoceptor-blocking agent, on arterial pressure and plasma renin activity, the degree of α-blockade induced by the drug being assessed by comparing the pressor response with that to a test dose of phenylephrine before and after prazosin administration, and (ii) the increases in plasma renin activity in response to isoprenaline before and during the prazosin-induced α-blockade. 2. Twenty minutes after the infusion of prazosin, when the pressor response to phenylephrine was reduced by 80% with respect to control, (i) mean arterial pressure was practically unchanged, (ii) plasma renin activity was almost doubled and (iii) the increases in plasma renin activity in response to isoprenaline were significantly greater, both in absolute and percentage values, than those observed before prazosin. 3. The increments in baseline plasma renin activity induced by prazosin in the absence of decrease in arterial pressure and the enhancement in renin responsiveness to the β-adrenoceptor stimulus suggest that, in man, the juxtaglomerular α1-adrenoceptors exert a direct, suppressive action on renin release.

Pressor response from rostral dorsomedial medulla is mediated by excitatory amino acid receptors in rostral VLM

1994 ◽  
Vol 267 (1) ◽  
pp. R309-R315 ◽  
Author(s):  
Y. Hirooka ◽  
J. W. Polson ◽  
R. A. Dampney
Keyword(s):  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Amino Acid Receptors ◽  
Control Value ◽  
Afferent Fibers ◽  
Pressor Responses ◽  
Before And After ◽  
Stimulation Of

Excitatory amino acid (EAA) receptors in the rostral part of the ventrolateral medulla (VLM) have been shown to mediate pressor responses elicited by stimulation of various peripheral afferent fibers as well as other central nuclei. This study tested the hypothesis that these receptors are a critical component in the central pathway mediating the powerful pressor response that is produced by stimulation of a group of neurons within a circumscribed region in the rostral dorsomedial medulla (RDM). In anesthetized rabbits, the pressor response elicited by unilateral microinjection of glutamate into this RDM region was measured before and after injection of kynurenic acid (Kyn), a broad-spectrum EAA receptor antagonist, into the physiologically identified pressor region of either the ipsilateral or contralateral rostral VLM. The pressor response to RDM stimulation was greatly reduced (to 24 +/- 4% of control) 5-10 min after injection of Kyn (but not the vehicle solution) into the ipsilateral rostral VLM; this response returned completely to its control value within 30-60 min after Kyn injection. By contrast, after Kyn injection into the contralateral rostral VLM, the pressor response to RDM stimulation was not affected (106 +/- 15% of control). The results indicate that the descending pressor pathway from the RDM to the spinal cord is mediated by EAA receptors in the rostral VLM pressor region. Furthermore, the pathway from the RDM to the rostral VLM is predominantly, if not exclusively, ipsilateral.

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