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.

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.

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.

Hemodynamic effects ofl-glutamate in NTS of conscious rats: a possible role of vascular nitrosyl factors

1998 ◽  
Vol 274 (4) ◽  
pp. H1066-H1074 ◽  
Author(s):  
Eduardo Colombari ◽  
Robin L. Davisson ◽  
Richard A. Shaffer ◽  
William T. Talman ◽  
Stephen J. Lewis
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Pressor Response ◽  
Nitric Oxide Synthesis ◽  
Hemodynamic Effects ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Sympathetic Nervous

This study examined peripheral mechanisms responsible for changes in mean arterial blood pressure, heart rate, and renal, mesenteric, and hindquarter vascular resistances produced by microinjections of l-glutamate (l-Glu) into the nucleus tractus solitarii (NTS) of conscious rats. Microinjection ofl-Glu produced an initial pressor response, bradycardia, and vasoconstriction in each vascular bed. Subsequent hindquarter vasodilation was observed. After prazosin was administered, l-Glu produced initial hypotension that was probably due to reduced cardiac output. This hypotension was followed by hindquarter vasodilation. Inhibition of nitric oxide synthesis did not affect the initial hypotension or bradycardia in rats treated with prazosin, but the first microinjection of l-Glu after administration of prazosin and N G-nitro-l-arginine methyl ester (l-NAME) produced significantly greater hindquarter vasodilation than after administration of prazosin alone. Second and third microinjections ofl-Glu produced significantly smaller hindquarter vasodilation. We conclude that 1) hemodynamic effects produced by microinjection of l-Glu into the NTS of conscious rats involves activation of the sympathetic nervous system and 2) release of preformed nitrosyl factors may mediate vasodilation in the hindquarter vascular bed.

scholarly journals Sex- and age-based differences in the effect of central serotonin on arterial blood pressure regulation

2020 ◽  
Vol 129 (6) ◽  
pp. 1310-1323
Author(s):  
Jennifer L. Magnusson ◽  
Craig A. Emter ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Nrem Sleep ◽  
Blood Pressure Regulation ◽  
Pressure Regulation ◽  
Adult Rats ◽  
Arterial Blood ◽  
Serotonin Neurons ◽  
Older Males

The role of serotonin in arterial blood pressure (ABP) regulation across states of vigilance is unknown. We hypothesized that adult rats devoid of CNS serotonin (TPH2−/−) have low ABP in wakefulness and NREM sleep, when serotonin neurons are active. However, TPH2−/− rats experience higher ABP than TPH2+/+ rats in wakefulness and REM only, a phenotype present only in older males and not females. CNS serotonin may be critical for preventing high ABP in males with aging.

scholarly journals Accumulation of Prostacyclin in Rat Brain during Haemorrhagic Hypotension—Possible Role of PGI2 in Autoregulation

1984 ◽  
Vol 4 (1) ◽  
pp. 107-109 ◽  
Author(s):  
E. Shohami ◽  
A. Sidi
Keyword(s):  
Blood Pressure ◽  
Steady State ◽  
Control Group ◽  
Prostaglandin E ◽  
Cortical Tissue ◽  
Arterial Blood ◽  
Haemorrhagic Hypotension ◽  
Potent Vasodilator ◽  
Prostaglandin F

The effect of haemorrhagic hypotension on the levels of prostaglandin E2 (PGE2), thromboxane B2 (TXB2), and 6-keto prostaglandin F1α (6-keto-PGF1α) in cortical tissue of rats was studied. Lightly anesthetized rats were subjected to steady-state hypotension for 15 min, with a mean arterial blood pressure of 80, 60, and 40 mm Hg, and compared to a control group of normotensive rats. No significant change was found in the levels of PGE2 and TXB2. The level of 6-keto-PGF1α increased from 7.8 ± 0.9 to 14.1 ± 1.9 pg/mg protein (p < 0.02) at 80 mm Hg. Our findings suggest that prostacyclin, which is a potent vasodilator, might play a role in setting the lower limit of the autoregulation range.

Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

scholarly journals Role of the medulla oblongata in normal and high arterial blood pressure regulation: the contribution of Escola Paulista de Medicina - UNIFESP

2009 ◽  
Vol 81 (3) ◽  
pp. 589-603 ◽  
Author(s):  
Sergio L. Cravo ◽  
Ruy R. Campos ◽  
Eduardo Colombari ◽  
Mônica A. Sato ◽  
Cássia M. Bergamaschi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Medulla Oblongata ◽  
Neural Circuits ◽  
Ventrolateral Medulla ◽  
Vasomotor Tone ◽  
Arterial Blood ◽  
Pathological Conditions ◽  
De Medicina

Several forms of experimental evidence gathered in the last 37 years have unequivocally established that the medulla oblongata harbors the main neural circuits responsible for generating the vasomotor tone and regulating arterial blood pressure. Our current understanding of this circuitry derives mainly from the studies of Pedro Guertzenstein, a former student who became Professor of Physiology at UNIFESP later, and his colleagues. In this review, we have summarized the main findings as well as our collaboration to a further understanding of the ventrolateral medulla and the control of arterial blood pressure under normal and pathological conditions.

scholarly journals Rostral ventral medulla 5-HT1A receptors selectively inhibit the somatosympathetic reflex

2001 ◽  
Vol 280 (5) ◽  
pp. R1261-R1268 ◽  
Author(s):  
Takashi Miyawaki ◽  
Ann K. Goodchild ◽  
Paul M. Pilowsky
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Selective Inhibition ◽  
Inhibitory Effect ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Potent Inhibition ◽  
Somatosympathetic Reflex

The role of the 5-hydroxytryptamine (5-HT1A) receptors in the rostral ventrolateral medulla (RVLM) on somatosympathetic, baroreceptor, and chemoreceptor reflexes was examined in anesthetized rats. Microinjection of the selective 5-HT1A agonist 8-hydroxy-di- n-propylamino tetralin (8-OH-DPAT) decreased arterial blood pressure and splanchnic sympathetic nerve activity (SNA). Electrical stimulation of the hindlimb evoked early and late excitatory sympathetic responses. Bilateral microinjection in the RVLM of 8-OH-DPAT markedly attenuated both the early and late responses. This potent inhibition of the somatosympathetic reflex persisted even after SNA and arterial blood pressure returned to preinjection levels. Preinjection of the selective 5-HT1A antagonist NAN-190 in the RVLM blocked the sympathoinhibitory effect of 8-OH-DPAT and attenuated the inhibitory effect on the somatosympathetic reflex. 8-OH-DPAT injected in the RVLM did not affect baroreceptor or chemoreceptor reflexes. Our findings suggest that activation of 5-HT1A receptors in the RVLM exerts a potent, selective inhibition on the somatosympathetic reflex.

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.

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