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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of hypercapnia on plasma renin concentration and blood pressure were studied in anaesthetized dogs, untreated and after pretreatment with guanethidine, propranolol or prazosin. An increase in plasma renin concentration which accompanied hypercapnia in untreated dogs was completely suppressed by pretreatment with guanethidine or propranolol. Prazosin significantly reduced but did not abolish renin release during hypercapnia. The pressor response normally occurring during hypercapnia was abolished by propranolol and reversed by guanethidine and prazosin.
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PMID:Participation of the sympathetic and the renin--angiotensin systems in blood pressure control during hypercapnia in the anaesthetized dog. 2 75

Widely distributed throughout the heart is a network of fibers connected to the medullary cardiovascular centers by nonmedullated vagal afferent fibers. When the traffic in these fibers is interrupted by vagal cooling, and the input from the arterial baroreceptors is prevented, the arterial blood pressure increases. Thus, these receptors act to inhibit tonically the vasomotor center. The receptors in the atria alter their rate of discharge with changes in atrial transmural pressure and contractility and are most active during end-inspiration and early expiration when the transmural pressure is maximal. The receptors in the ventricles respond to changes in ventricular end-diastolic pressure (preload), to the pressure generated during systole (afterload) and to changes in ventricular contractility. The cardiac mechanoreceptors have an equal or greater effect on the renal bed than the arterial mechanoreceptors and this effect is enhanced by hypercapnia. In animals, the cardiac mechanoreceptors have less control of the muscle vessels than the arterial mechanoreceptors, but the reverse is true in man. Both the cardiac and arterial mechanoreceptors can modulate the output of renin from the kidney, but the cardiac mechanoreceptors are more sensitive to small changes in blood volume. During coronary occlusion, in association with the bulging of the ischemic myocardium, the rate of discharge of these cardiac receptors is greatly increased.
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PMID:Cardiac receptors: normal and disturbed function. 38 68

Water balance is tightly regulated within a tolerance of less than 1 percent by a physiologic control system located in the hypothalamus. Body water homeostasis is achieved by balancing renal and nonrenal water losses with appropriate water intake. The major stimulus to thirst is increased osmolality of body fluids as perceived by osmoreceptors in the anteroventral hypothalamus. Hypovolemia also has an important effect on thirst which is mediated by arterial baroreceptors and by the renin-angiotensin system. Renal water loss is determined by the circulating level of the antidiuretic hormone, arginine vasopressin (AVP). AVP is synthesized in specialized neurosecretory cells located in the supraoptic and paraventricular nuclei in the hypothalamus and is transported in neurosecretory granules down elongated axons to the posterior pituitary. Depolarization of the neurosecretory neurons results in the exocytosis of the granules and the release of AVP and its carrier protein (neurophysin) into the circulation. AVP is secreted in response to a wide variety of stimuli. Change in body fluid osmolality is the most potent factor affecting AVP secretion, but hypovolemia, the renin-angiotensin system, hypoxia, hypercapnia, hyperthermia and pain also have important effects. Many drugs have been shown to stimulate the release of AVP as well. Small changes in plasma AVP concentration of from 0.5 to 4 muU per ml have major effects on urine osmolality and renal water handling.
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PMID:The clinical physiology of water metabolism. Part I: The physiologic regulation of arginine vasopressin secretion and thirst. 39 80

This investigation was undertaken to determine the nature of acute alterations in renal function following the production of hypoxemia, hypercarbia, and acidosis in newborn piglets 6-96 hr of age. After completion of the surgical procedure piglets were allowed to recover from the effects of anesthesia. When respiratory dead space was increased arterial oxygen tension decreased whereas arterial carbon dioxide tension and hydrogen ion concentration increased. There was little change in glomerular filtration rate. Total renal blood flow decreased and renal vascular resistance increased significantly (504 +/- 78 mm Hg/liter/mm/m2 to 1422 +/- 504). There was no change in distribution of intrarenal blood flow. Sodium excretion and urinary flow rate demonstrated significant parallel increases following the increase in dead space. Plasma renin concentration increased from 67 to 110 ng/ml.
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PMID:Effects of asphyxia on renal function in the newborn piglet. 58 Apr 50

Hypoxia and the hypercapnia were produced in anesthetized dogs by artificial respiration with appropriate gas mixtures, and a study was conducted of the effects of these conditions on various metabolic parameters, viz. catecholamines, renin activity, lactate, pyruvate, cortisol, non-esterified free fatty acids (FFA), and ammonia, in the plasma of the arterial blood. Hypercapnia caused a distinct increase in catecholamine concentrations, renin activity and ammonia, and a decrease in lactate and pyruvate; cortisol and FFA levels were only slightly altered. Hypoxia increased lactate, pyruvate and--though only to a slight extent--FFA, cortisol and NH3. The changes induced by hypercapnia were chiefly attributable to activation of the sympathico-adrenal system; those induced by hypoxia were not.
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PMID:[Metabolic effects of acute experimental hypoxia and hypercapnia]. 92 42

1. The blood-bathed organ technique was used to study the release of catecholamines, angiotensin II and prostaglandin-like (PL) substances into the circulation during hypercapnia and after haemorrhage in anaesthetized dogs. 2. Elevated blood concentrations of noradrenaline, angiotensin II and prostaglandin-like substances have been detected during both experimental conditions. 3. The rise of arterial blood pressure during hypercapnia and after haemorrhage was associated with elevated concentrations of angiotensin II in the blood and could be abolished by inhibition of the angiotensin I-converting enzyme with SQ 20881. 4. The compensation of arterial pressure during both stresses was significantly impaired by release of prostaglandin-like substances; it could be restored by inhibition of prostaglandin biosynthesis with indomethacin. 5. The results indicate that activation of the renin-angiotensin system represents the major humoral mechanism for the maintenance of arterial pressure during hypercapnic acidosis and after haemorrhage.
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PMID:Humoral response and blood pressure regulation during hypercapnia and haemorrhage in dogs. 107 98

In dogs, plasma renin activity (PRA) was increased by anesthesia, by hypercapnia and by extreme hypoxia (paO2 47.6 mm Hg). Relatively moderate hypoxia (paO2 47.6 mm Hg) and artificial respiration had no appreciable influence on PRA. It appears that the sympathomimetic stimulus of CO2 has an important bearing on PRA.
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PMID:[Proceedings: Experimentally induced effects on the plasma renin activity]. 121 77

To evaluate the role of certain plasma biosubstances on the development of pulmonary hypertension and shock during severe hypoxia, hypercapnia and acidosis, plasma renin activity (PRA), angiotensin II (ATII), angiotensin converting enzyme (ACE), TXB2 and 6-Keto-PGF1 alpha (the stable metabolites of TXA2 and PGI2) were assayed in blood from pulmonary artery and aorta in seven pigs. Pulmonary arterial pressure (PAP) was monitored via Swan-Ganz catheter. During hypoxic and hypercapnic ventilation, PaO2 dropped to 4.7 kPa, PaCO2 rose to 21.1 kPa, pH dropped to 6.82, PAP increased from 2.43 +/- 0.06 to 4.46 +/- 0.45 kPa when acidotic shock developed (all P less than 0.05). Meanwhile ATII levels rose (all P less than 0.05). PRA significantly increased during acidotic shock as compared with normal ventilation (P less than 0.02). ACE dropped significantly (P less than 0.05), TXB2 and 6-keto-PGF1 alpha showed no significant change before and after hypoxic and hypercapnic ventilation.
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PMID:[Plasma renin activity, angiotensin II, angiotensin converting enzyme, thromboxane A2 and prostacyclin I2 levels in pigs with severe hypoxia and hypercapnea and acidosis shock]. 132 48

Changes in arterial pressure commonly accompany respiratory adaptations. The purpose of this study was to determine, in awake dogs (n = 6), the degree to which small acute decreases in arterial pressure affect ventilation and acid-base balance. Mean arterial pressure (MAP) was reduced by 6 +/- 2, 10 +/- 3, and 16 +/- 2% by intravenous infusion of sodium nitroprusside for sequential 20-min periods. In another experiment, the ventilatory response to hypercapnia was determined during MAP reduction of 16 +/- 3%. Step reductions in MAP were accompanied by increases in minute ventilation (maximum increase 152 +/- 75%) and step reductions in arterial PCO2 (PaCO2; maximum reduction -4.8 +/- 0.8 Torr). Although eupneic PaCO2 threshold was lowered during MAP reduction, ventilatory sensitivity to CO2 remained unchanged. Despite the lowered PaCO2, arterial [H+] remained constant (acid-base balance was maintained) as a result of a concurrent decrease in strong ion difference. Plasma renin activity increased during MAP reduction (93 +/- 39%) and may have contributed to the increase in minute ventilation, inasmuch as angiotensin II can stimulate respiration by a central mechanism. Evidence is provided that nitroprusside is unlikely to be a primary factor in these hypotensive responses. We conclude that relatively modest decreases in MAP have a consistent stimulatory effect on respiratory control. Therefore it is important to take into account effects of small changes in MAP when interpreting mechanisms for respiratory responses in awake animals.
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PMID:Ventilation is stimulated by small reductions in arterial pressure in the awake dog. 144 3

Late-gestation fetal sheep respond to slow hemorrhage with increases in plasma concentrations of adrenocorticotropic hormone (ACTH), hydrocortisone, arginine vasopressin (AVP), and plasma renin activity (PRA) that correlate to the acidemia and hypercapnia also produced by hemorrhage. This study was designed to investigate the role of peripheral chemoreceptors in the mediation of these responses. Chronically catheterized fetal sheep were left intact or were subjected to bilateral section of cervical vagosympathetic trunks and carotid sinus nerves. At least 5 days after surgical preparation (between 121 and 138 days of gestation) fetuses were bled at a rate of 11 ml/10 min for 2 h. Denervated fetuses were studied with or without simultaneous infusion of phenylephrine. Denervation exaggerated the decrease in mean arterial pressure and arterial pH and the increase in arterial PCO2 during hemorrhage. Infusion of phenylephrine in the denervated fetuses prevented the decrease in blood pressure and reduced the magnitudes of changes in blood gases. Fetal plasma ACTH, hydrocortisone, and PRA responses to the hemorrhage were exaggerated in the denervated fetuses (not infused with phenylephrine) compared with the intact fetuses. Phenylephrine infusion attenuated the ACTH response and inhibited the AVP response but did not alter the PRA response. We conclude that the sectioned fibers are important for the maintenance of blood pressure and blood gases during hemorrhage and that the PRA, AVP, and ACTH responses to slow hemorrhage are not mediated by peripheral chemoreceptors.
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PMID:Reflex control of fetal arterial pressure and hormonal responses to slow hemorrhage. 173 13


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