Interaction of bradykinin and prostaglandin E1 on cardiac pressor reflex and sympathetic afferents

1986 ◽  
Vol 250 (5) ◽  
pp. R815-R822 ◽  
Author(s):  
T. Nerdrum ◽  
D. G. Baker ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Blood Pressure ◽  
Prostaglandin E1 ◽  
Pressor Response ◽  
Interactive Effect ◽  
Small Reduction ◽  
Arterial Blood ◽  
Repeated Applications ◽  
Pressor Reflex ◽  
Cardiac Afferents ◽  
Afferent Response

Bradykinin applied to the epicardium stimulates cardiac sympathetic afferents and evokes a reflex increase in arterial blood pressure. In anesthetized cats we examined the potentiation of these effects by prostaglandin E1 (PGE1) applied to the ventricular epicardium. We recorded cardiac afferent impulses from the second to the fifth left thoracic sympathetic rami. PGE1 (0.1 microgram/ml) alone had little effect on blood pressure, but it significantly increased the pressor response to bradykinin, and it reduced or abolished tachyphylaxis to repeated applications of bradykinin. Both mechanosensitive and chemosensitive sympathetic cardiac afferents were stimulated by bradykinin. Indomethacin (intravenous) caused a small reduction in the afferent response to bradykinin. Epicardial application of PGE1 significantly increased the response (magnitude and duration) of chemosensitive endings to bradykinin but not that of mechanosensitive endings; however, PGE1 abolished the tachyphylaxis of both chemosensitive and mechanosensitive endings to repeated applications of bradykinin. Because both bradykinin and prostaglandins are released in the ischemic myocardium, their interactive effect on cardiac sympathetic afferents could play a part in the sensory and reflex responses to myocardial ischemia.

Nitric oxide modulates sympathoexcitatory cardiac-cardiovascular reflexes elicited by bradykinin

2001 ◽  
Vol 281 (5) ◽  
pp. H2010-H2017 ◽  
Author(s):  
S. C. Tjen-A-Looi ◽  
N. T. Phan ◽  
J. C. Longhurst
Keyword(s):  
Nitric Oxide ◽  
Pressor Response ◽  
Reflex Response ◽  
Cardiovascular Reflexes ◽  
Control Group ◽  
Neural Modulation ◽  
Arterial Blood ◽  
Nos Inhibitor ◽  
Pressor Reflex ◽  
Cardiac Afferents

A number of studies have demonstrated an important role for nitric oxide (NO) in central and peripheral neural modulation of sympathetic activity. To assess the interaction and integrative effects of NO release and sympathetic reflex actions, we investigated the influence of inhibition of NO on cardiac-cardiovascular reflexes. In anesthetized, sinoaortic-denervated and vagotomized cats, transient reflex increases in arterial blood pressure (BP) were induced by application of bradykinin (BK, 0.1–10 μg/ml) to the epicardial surface of the heart. The nonspecific NO synthase (NOS) inhibitor N G-monomethyl-l-arginine (l-NMMA, 10 mg/kg iv) was then administered and stimulation was repeated. l-NMMA increased baseline mean arterial pressure (MAP) from 129 ± 8 to 152 ± 9 mmHg and enhanced the change in MAP in response to BK from 32 ± 3 to 39 ± 5 mmHg ( n = 9, P < 0.05). Pulse pressure was significantly enhanced during the reflex response from 6 ± 4 to 27 ± 6 mmHg after l-NMMA injection due to relatively greater potentiation of the rise in systolic BP. Both the increase in baseline BP and the enhanced pressor reflex were reversed by l-arginine (30 mg/kg iv). Because l-NMMA can inhibit both brain and endothelial NOS, the effects of 7-nitroindazole (7-NI, 25 mg/kg ip), a selective brain NOS inhibitor, on the BK-induced cardiac-cardiovascular pressor reflex also were examined. In contrast to l-NMMA, we observed significant reduction of the pressor response to BK from 37 ± 5 to 18 ± 3 mmHg 30 min after the administration of 7-NI ( n = 9, P < 0.05), an effect that was reversed by l-arginine (300 mg/kg iv, n = 7). In a vehicle control group for 7-NI (10 ml of peanut oil ip), the pressor response to BK remained unchanged ( n = 6, P > 0.05). In conclusion, neuronal NOS facilitates, whereas endothelial NOS modulates, the excitatory cardiovascular reflex elicited by chemical stimulation of sympathetic cardiac afferents.

Augmentation of the exercise pressor reflex in prehypertension: roles of the muscle metaboreflex and mechanoreflex

2013 ◽  
Vol 38 (2) ◽  
pp. 209-215 ◽  
Author(s):  
Hyun-Min Choi ◽  
Charles L. Stebbins ◽  
Og-Taeg Lee ◽  
Hosung Nho ◽  
Joon-Hee Lee ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Percentage Increase ◽  
Muscle Metaboreflex ◽  
Exercise Pressor Reflex ◽  
Arterial Blood ◽  
Static Contraction ◽  
Pressor Reflex

This study investigated the hemodynamic mechanisms underlying the exaggerated blood pressure response to muscle contraction in prehypertensive humans and the potential role of skeletal muscle metabo- and mechanoreceptors in this response. To accomplish this, changes in peak mean arterial blood pressure (ΔMAP), cardiac output, and total peripheral resistance (ΔTPR) were compared between prehypertensive (n = 23) and normotensive (n = 19) male subjects during 2 min of static contraction (at 50% of maximal tension), 2 min of postexercise muscle ischemia (metaboreflex), and 1 min of passive dorsiflexion of the foot (tendon stretch, mechanoreceptor reflex). These variables were assessed before and during the interventions. Percentage increases from baseline in MAP and TPR in response to the exercise pressor reflex were augmented in the prehypertensives, compared with the normotensives (44% ± 5% vs. 33% ± 4% and 34% ± 15% vs. 2% ± 8%, respectively) (p < 0.05). Metaboreflex-induced increases in MAP and TPR were also augmented in the prehypertensives (28% ± 5% vs. 14% ± 4% and 36% ± 12% vs. 14% ± 9%, respectively) (p < 0.05). In response to the mechanoreflex, no differences in the percentage increase in MAP or TPR were seen between groups. The results indicate that the reflex pressor response to static contraction is augmented in prehypertension and suggest that this phenomenon is due, at least in part, to enhanced activation of metaboreceptors.

Blood pressure during routine activity, stress, and feeding in black racer snakes (Coluber constrictor)

1993 ◽  
Vol 264 (1) ◽  
pp. R79-R84 ◽  
Author(s):  
J. N. Stinner ◽  
D. L. Ely
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Acute Stress ◽  
Pressor Response ◽  
Routine Activity ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Coluber Constrictor ◽  
S Peak ◽  
Hematological Changes

The pressor response to normal daily behaviors and acute stress was studied in black racer snakes (Coluber constrictor) at 30 degrees C. In addition, hematological changes during the stress response were assessed. Mean nighttime systemic arterial blood pressure (SABP) in undisturbed snakes was lower than daytime pressure (26 +/- 3 vs. 32 +/- 9 mmHg, P < 0.001). When snakes were fed mice, SABP increased 3.5- to 4-fold and heart rate increased approximately 3-fold above resting values within approximately 30 s (peak SABP, 99 +/- 18 mmHg; peak heart rate, 99 +/- 12 beats/min). Killing and ingesting the mice required 6-15 min, during which time mean SABP and heart rate were 84 +/- 16 mmHg and 92 +/- 12 beats/min. Pulmonary blood pressure also increased but remained 40-50 mmHg lower than SABP. During stress elicited by tapping the snakes for 5-8 min, heart rate was 94 +/- 6 beats/min but SABP averaged only 44 +/- 11 mmHg. Plasma norepinephrine and epinephrine increased 51- and 26-fold. Plasma glucose increased 58%, hematocrit increased 19%, and plasma volume decreased 19%. It is concluded that blood pressure is markedly affected by behavior and that the sympathetic nervous system appears to play a key role.

Cardiovascular effects of human recombinant interleukin-1 beta in conscious rats

1994 ◽  
Vol 266 (4) ◽  
pp. R1148-R1153 ◽  
Author(s):  
A. Bataillard ◽  
J. Sassard
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Interleukin 1 ◽  
Renin Angiotensin System ◽  
Cardiovascular Effects ◽  
Interleukin 1 Beta ◽  
Pronounced Increase ◽  
Arterial Blood

Cardiovascular effects of human recombinant interleukin-1 beta (hrIL-1 beta) were investigated in normotensive rats using a computerized analysis of arterial blood pressure in conscious, unrestrained animals. Intravenous injection of hrIL-1 beta induced a rapid and short-lasting rise in blood pressure associated with a first slight tachycardia followed by a second sustained and pronounced increase in heart rate. These effects occurred in a dose-related manner. Pretreatment with a converting-enzyme inhibitor (perindopril) did not modify the hrIL-1 beta-induced increase in blood pressure. Blockade of beta 1-adrenoceptors (atenolol) prevented the tachycardia, but did not significantly affect the pressor response to hrIL-1 beta. On the contrary, the hrIL-1 beta-induced increase in blood pressure was inhibited by an alpha 1-adrenoceptor antagonist (prazosin), whereas the tachycardia was untouched. Finally, pretreatment with a cyclooxygenase inhibitor (indomethacin) completely abolished the cardiovascular response to hrIL-1 beta. These results suggest that the hrIL-1 beta-induced pressor response and associated tachycardia require the synthesis of prostaglandins and involve a sympathetic nervous system activation but do not depend on the renin-angiotensin system.

In vitro and in vivo inhibition of renin by fatty acids.

1978 ◽  
Vol 234 (6) ◽  
pp. E593 ◽  
Author(s):  
T A Kotchen ◽  
W J Welch ◽  
R T Talwalkar
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Linoleic Acid ◽  
Angiotensin Ii ◽  
Neutral Lipids ◽  
Pressor Response ◽  
Arterial Blood ◽  
Arachidonic Acids

Circulating neutral lipids inhibit the in vitro renin reaction. To identify the inhibitor(s), free fatty acids were added to human renin and homologous substrate. Capric, lauric, palmitoleic, linoleic, and arachidonic acids each inhibited the rate of angiotensin I production in vitro (P less than 0.01). Inhibition by polysaturated fatty acids (linoleic and arachidonic) was less (P less than 0.01) after catalytic hydrogenation of the double bonds. To evaluate an in vivo effect of renin inhibition intra-arterial blood pressure responses to infusions of renin and angiotensin II (5.0 microgram) were measured in anephric rats (n = 6) before and after infusion of linoleic acid (10 mg iv). Mean increase of blood pressure to angiotensin II before (75 mmHg +/- 9) and after (90 +/- 12) linoleic acid did not differ (P greater than 0.05). However, the pressor response to renin after linoleic acid (18 +/- 3) was less (P less than 0.00)) than that before (102 +/- 13). In summary, several fatty acids inhibit the in vitro renin reaction, and in part inhibition is dependent on unsaturation. Linoleic acid also inhibits the in vivo pressor response to renin. These results suggest that fatty acids may modify the measurement of plasma renin activity and may also affect angiotensin production in vivo.

Muscle chemoreflex alters vascular conductance in nonischemic exercising skeletal muscle

1994 ◽  
Vol 77 (6) ◽  
pp. 2761-2766 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
P. S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Response To Exercise ◽  
Muscle Chemoreflex

Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.

Effect of norepinephrine on plasma free fatty acids in dogs treated with reserpine

1963 ◽  
Vol 205 (1) ◽  
pp. 57-59 ◽  
Author(s):  
Francois M. Abboud ◽  
Michael G. Wendling ◽  
John W. Eckstein
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Arterial Blood Pressure ◽  
Pressor Response ◽  
Maximal Increase ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Plasma Ffa

Some adrenergic blocking drugs reduce the mobilization of free fatty acids (FFA) in response to administration of catecholamines. The present experiments were done to see if potentiation of the pressor effect of norepinephrine by reserpine is accompanied by a greater increase in plasma FFA. Norepinephrine was infused intravenously into 16 anesthetized dogs. Eight of them had been treated with reserpine, 0.25 mg/kg daily, intraperitoneally for 2 days; the others were not treated. Arterial blood samples were drawn before, during, and after norepinephrine for determination of plasma FFA concentrations. Systemic arterial blood pressure was measured continuously. In the treated animals the maximal increase in arterial blood pressure as well as the progressive increments in FFA concentration were greater than in the untreated dogs. The experiments indicate that potentiation of the pressor response to norepinephrine after reserpine is accompanied by a greater FFA response.

Central sympathetic outflow to skeletal muscle: the major link between non-esterified fatty acids and elevated blood pressure?

2009 ◽  
Vol 118 (1) ◽  
pp. 43-45 ◽  
Author(s):  
Markus Schlaich
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Pressor Response ◽  
The Metabolic Syndrome ◽  
Arterial Blood ◽  
Esterified Fatty Acids ◽  
System Activation ◽  
Central Sympathetic Outflow ◽  
Sympathetic Nervous System Activation

Sympathetic nervous system activation is a hallmark of several conditions associated with an adverse prognosis, including hypertension and the metabolic syndrome. Proposed mediators of increased sympathetic drive include hyperinsulinaemia, leptin, NEFAs (non-esterified fatty acids), pro-inflammatory cytokines, baroreflex impairment and others. The role of NEFAs appears to be of particular importance given the increased levels observed in human obesity and the experimental results linking the NEFA-induced pressor response to sympathetic activation. Findings from human studies have yielded conflicting results with regards to a sympathetically mediated association between NEFAs and elevated arterial blood pressure. In the present issue of Clinical Science, Florian and Pawelczyk present some interesting results obtained from a small number of healthy normotensive lean volunteers who were exposed to NEFA infusion and cardiovascular and sympathetic monitoring using state of the art methodology that appears to be in support of such a link. However, several methodological and conceptual considerations need to be taken into account when interpreting the results from this study. Put into perspective, the case for a substantial sympathetically mediated pressor response to NEFA infusion does not appear to be a very strong one.

Cardiovascular control during voluntary static exercise in humans with tetraplegia

2004 ◽  
Vol 97 (6) ◽  
pp. 2077-2082 ◽  
Author(s):  
Makoto Takahashi ◽  
Akihiro Sakaguchi ◽  
Kanji Matsukawa ◽  
Hidehiko Komine ◽  
Kotaro Kawaguchi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cervical Spinal Cord ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Voluntary Contraction ◽  
Static Exercise ◽  
Arm Exercise ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was 1) to investigate whether an increase in heart rate (HR) at the onset of voluntary static arm exercise in tetraplegic subjects was similar to that of normal subjects and 2) to identify how the cardiovascular adaptation during static exercise was disturbed by sympathetic decentralization. Mean arterial blood pressure (MAP) and HR were noninvasively recorded during static arm exercise at 35% of maximal voluntary contraction in six tetraplegic subjects who had complete cervical spinal cord injury (C6-C7). Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were estimated by using a Modelflow method simulating aortic input impedance from arterial blood pressure waveform. In tetraplegic subjects, the increase in HR at the onset of static exercise was blunted compared with age-matched control subjects, whereas the peak increase in HR at the end of exercise was similar between the two groups. CO increased during exercise with no or slight decrease in SV. MAP increased approximately one-third above the control pressor response but TPR did not rise at all throughout static exercise, indicating that the slight pressor response is determined by the increase in CO. We conclude that the cardiovascular adaptation during voluntary static arm exercise in tetraplegic subjects is mainly accomplished by increasing cardiac pump output according to the tachycardia, which is controlled by cardiac vagal outflow, and that sympathetic decentralization causes both absent peripheral vasoconstriction and a decreased capacity to increase HR, especially at the onset of exercise.

Attenuated pulmonary pressor response to hypoxia in bar-headed geese

1984 ◽  
Vol 247 (2) ◽  
pp. R402-R403 ◽  
Author(s):  
F. M. Faraci ◽  
D. L. Kilgore ◽  
M. R. Fedde
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Control Mechanisms ◽  
Vascular Control ◽  
Pekin Ducks ◽  
Arterial Blood ◽  
O2 Partial Pressure ◽  
Unique Model ◽  
Pulmonary Arterial ◽  
Anser Indicus

We determined the pulmonary pressor response during hypoxia in bar-headed geese (Anser indicus), a species that flies at altitudes up to 9,000 m, and Pekin ducks (Anas platyrhynchos), a non-flyer. Mean pulmonary arterial blood pressure (PAP) and arterial O2 partial pressure (PaO2) were measured in unanesthetized birds acutely exposed to 21, 10, 5, and, in geese only, 4% O2. PAP in geese did not change as PaO2 was reduced from 95 to 46 Torr and rose only 3 mmHg when PaO2 was reduced to 28 Torr. The same PaO2 decline in ducks (99 to 29 Torr) resulted in an 11-mmHg rise in PAP. The data suggest that very little or no increase in pulmonary vascular resistance occurs in these geese during hypoxia. This bird may provide a unique model in which to study pulmonary vascular control mechanisms.

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