The Involvement of Medullary Reticular Formation in the Hypotensive Effect of Extracts from Seeds of Cassia Tora

1976 ◽  
Vol 04 (04) ◽  
pp. 383-389 ◽  
Author(s):  
Samuel H. H. Chan ◽  
Anthony Koo ◽  
K. M. Li
Keyword(s):  
Blood Pressure ◽  
Reticular Formation ◽  
Hypotensive Effect ◽  
Cardiovascular Reflexes ◽  
Vasomotor Tone ◽  
Medullary Reticular Formation ◽  
Cassia Tora ◽  
Induced Hypotension ◽  
Arterial Blood

In pentobarbital anesthezied rats, the medial portion of the medullary reticular formulation has been identified to be directly involved in the hypotensive effect of extracts from the seeds of Cassia tora. This conclusion was drawn from the observed decrease in arterial blood pressure following local injection of extracts of this herb into this reticular site and from its inability to promote hypotension when the same reticular site has been electrolytically lesioned. The role of the medullary reticular formation in the Cassia tora-induced hypotension was suggested to be one which modulates the basic cardiovascular reflexes, favoring a decrease in vasomotor tone.

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.

Captopril-induced hypotension is inhibited by the bradykinin blocker HOE-140 in Na(+)-depleted marmosets

1995 ◽  
Vol 269 (4) ◽  
pp. H1221-H1228
Author(s):  
M. J. Panzenbeck ◽  
C. L. Loughnan ◽  
J. B. Madwed ◽  
R. J. Winquist ◽  
S. E. Fogal
Keyword(s):  
Blood Pressure ◽  
Hypotensive Effect ◽  
Induced Hypotension ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Arterial Blood ◽  
Vehicle Treatment ◽  
Hoe 140 ◽  
B2 Receptors ◽  
Hypotensive Response

Inhibition of angiotensin-converting enzyme (ACE) inhibits formation of angiotensin II and, by inhibition of kinin metabolism, may also increase vascular bradykinin. The present experiments were done in sodium-depleted, conscious, unrestrained marmosets (n = 5-11) to examine the contribution of bradykinin to ACE inhibitor-induced hypotension. Aortic blood pressure and heart rate (HR) were monitored via telemetry. After sodium depletion (low-sodium diet and furosemide), captopril (1 mg/kg po) caused a significant (P < 0.05) decrease in mean arterial blood pressure (MABP) (-34 +/- 3 mmHg, maximally, from 79 +/- 2 mmHg) but no change in HR compared with vehicle treatment. The bradykinin receptor antagonist HOE-140 (1 mg/kg sc) significantly inhibited the hypotensive response to captopril and caused marked tachycardia (+133 +/- 14 beats/min from 214 +/- 8 beats/min). HOE-140 (1 mg/kg sc) followed by vehicle administration had no effect on MABP but increased HR similarly. The hypotensive response to captopril was inhibited by HOE-140 regardless of the order of administration or the route of captopril administration (by mouth vs. subcutaneously). The hypotensive response to a renin inhibitor, A-72517 (3 mg/kg sc), was not inhibited by prior HOE-140 administration despite a similar HOE-140-induced tachycardia. These data suggest that the hypotensive effect of captopril in sodium-depleted, conscious marmosets is dependent on functional bradykinin B2 receptors. Also, blockade of B2 receptors uncovers marked tachycardia in this model, suggesting a tonic effect of bradykinin on control of HR in marmosets.

scholarly journals Mediation systems in bacterial lipopolysaccharide-induced hypotension and disseminated intravascular coagulation. I. The role of complement.

1975 ◽  
Vol 142 (6) ◽  
pp. 1570-1590 ◽  
Author(s):  
R J Ulevitch ◽  
C G Cochrane ◽  
P M Henson ◽  
D C Morrison ◽  
W F Doe
Keyword(s):  
Blood Pressure ◽  
Disseminated Intravascular Coagulation ◽  
Mononuclear Cells ◽  
Contrast Injection ◽  
Marked Contrast ◽  
Induced Hypotension ◽  
E Coli ◽  
Intravascular Coagulation ◽  
Arterial Blood

We have studied the role of complement in lipopolysaccharide (LPS)-induced hypotension and disseminated intravascular coagulation (DIC) by comparing the effects of injection of three preparations of LPS from E. Coli 0111:B4, S. minnesota Re595, and S. marcescens. Injections of nonlethal doses of these LPS preparations into normal rabbits produced decreases in mean arterial blood pressure during a 5-h period. When rabbits treated with cobra venom factor (CoF) to deplete C3 were injected with the various LPS preparations, mean arterial pressures fell at a rate and extent essentially identical to that observed in normal rabbits. Rabbits genetically deficient in C6 also demonstrated LPS-induced hypotensive changes. Only minimal, or no changes in plasma C3 levels or serum CH50 values were detected in normal rabbits after LPS injection. Hypotensive changes were also induced in rabbits when complement was rapidly activated by intravenous injection of CoF. In contrast to the hypotension induced by LPS, the fall in arterial pressure associated with the consumption of complement was short lived and required the rapid consumption of considerable amounts of C3. The occurrence of DIC noted in normal rabbits injected with each preparation of LPS was not inhibited in either rabbits treated with cobra factor or in C6-deficient rabbits. The DIC was most pronounced after injection of Re595 and S. marcescens LPS. Injection of the various LPS preparations produced a rapid disappearance of circulating neutrophils and mononuclear cells, which occurred with the same kinetics and to the same extent in normal, CoF-treated, and C6-deficient rabbits. Injection of either Re595 LPS or S. marcescens LPS produced a biphasic disappearance of circulating 51Cr-platelets. In contrast, injection of 0111:B4 LPS affected only slightly the rate of disappearance of 51Cr-platelets. Depletion of C3 by cobra factor treatment had no effect on the disappearance of platelets in animals injected with 0111:B4. In marked contrast cobra factor treatment greatly reduced the initial rapid disappearance of platelets in rabbits injected with either Re595 or S. marcescens LPS, but had no effect in the secondary disappearance phase.

Cardiovascular reflexes following lesions in medullary reticular formation

1965 ◽  
Vol 208 (2) ◽  
pp. 283-288 ◽  
Author(s):  
John W. Manning
Keyword(s):  
Blood Pressure ◽  
Reticular Formation ◽  
Tissue Injury ◽  
Cardiac Activity ◽  
Cardiovascular Reflexes ◽  
Medullary Reticular Formation ◽  
Cardiovascular Reflex ◽  
Vascular Reflex ◽  
Inferior Olivary ◽  
Stimulation Of

In 19 anesthetized cats acute destruction of large portions of the medullary reticular formation was achieved with the aid of a radio-frequency lesion maker. Midline structures were spared by confining the lesions to the dorsolateral medulla. Tissue injury extended from a level rostral to the inferior olivary complex to the obex. These lesions in the medullary vasomotor area did not alter significantly the cardiovascular reflex adjustments to bilateral occlusion of the carotid arteries or to the stimulation of the central end of the cut sciatic nerve. In addition, an increase in contractile force, heart rate, and blood pressure evoked by stimulation of pressor areas in the posterior hypothalamus could be obtained following the lesions. The preparations were critically dependent upon supramedullary connections to maintain vascular tone and circulatory reflex adjustments, for decerebration in the lesioned animal brought about a reduction in blood pressure and a loss of vascular reflex responses. These findings suggest that supramedullary centers exert tonic as well as phasic influences on vascular and cardiac activity that is independent of the medullary vasomotor area.

Decreases in arterial pressure activate oxytocin neurons in conscious rats

1997 ◽  
Vol 273 (4) ◽  
pp. R1474-R1483 ◽  
Author(s):  
Jennifer C. Schiltz ◽  
Gloria E. Hoffman ◽  
Edward M. Stricker ◽  
Alan F. Sved
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Plasma Levels ◽  
Plasma Osmolality ◽  
Hypotensive Effect ◽  
Drug Induced ◽  
Induced Hypotension ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Acute Hypotension

Hemorrhage and nonhypotensive hypovolemia are known to increase plasma levels of oxytocin (OT) and vasopressin (VP) in rats. The present experiments demonstrated that secretion of OT and VP also are stimulated by acute drug-induced hypotension. Injection of hydralazine abruptly decreased arterial blood pressure in conscious rats and induced Fos expression, a marker of neuronal activation, within OT and VP neurons in the hypothalamus. Hydralazine also elicited substantial increases in plasma levels of both OT and VP. Injection of chlorisondamine similarly elicited acute hypotension and increased plasma levels of OT and VP. Furthermore, when the hypotensive effect of chlorisondamine was blunted by coinfusion of phenylephrine, the induced increases in OT and VP were markedly attenuated. Across all treatments, arterial blood pressure was inversely related to plasma levels of OT and VP. Plasma osmolality was not increased by hydralazine, nor was there evidence of gastric malaise, two known stimuli for OT secretion in rats. These results suggest that arterial hypotension increases neurohypophysial release of OT and VP in conscious rats.

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.

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