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N C Gonzalez

Publications and source records attributed to N C Gonzalez.

At least 55 records · Page 3Linked to original sources
PubMed1984

Role of the renin-angiotensin system in hypertension after coarctation of the aorta.

The effect of inhibition of angiotensin I converting enzyme by captopril was studied in rats with aortic coarctation produced above the renal arteries. When captopril therapy was started before coarctation, blood pressure above the narrowing and the pressure difference across the coarctation were reduced, compared with values in animals with coarctation not given therapy. When captopril therapy was started 10 days after the coarctation, there was no effect on blood pressure. Plasma renin activity increased 24 hours after coarctation and returned to control levels by 5 days. Captopril caused an increase in renin activity and a decrease in plasma aldosterone concentrations. After 5 days, there was no difference in renin activity and plasma aldosterone levels between animals with coarctation given captopril therapy early and late and between appropriate controls. Our data suggest that the renin-angiotensin system is important in the early development but not in the maintenance of coarctation hypertension.

Animals↗
PubMed1983

Role of adrenals on development of pressure-induced myocardial hypertrophy.

The effect of coarctation of the abdominal aorta (AC) and of sham operation (SO) on the development of myocardial hypertrophy was studied in three groups of male rats, i.e., a group without treatment prior to AC or SO (untreated), a group with bilateral adrenalectomy (ADX) 5-7 days before AC or SO, and a group in which the adrenal medulla was removed (MDX) 5-7 days before AC or SO. MDX resulted in functional elimination of the adrenal medulla without apparent effect on cortical function. The animals were killed 7-10 days after AC or SO. AC produced carotid blood pressure (CBP) increases of 33, 31, and 25 mmHg in the untreated, ADX, and MDX groups, respectively. Ventricular weight (HW), ventricular RNA concentration, and RNA-to-DNA ratio increased significantly after AC only in the untreated and MDX groups. In the ADX group, hypertension was followed by an increase in HW that could be detected only after normalization for body weight. It is concluded that absence of the adrenal gland significantly reduces the development of pressure-induced myocardial hypertrophy. Apparently, this is due to the absence of the adrenal cortex and not absence of the adrenal medulla.

Adrenal Glands↗
PubMed1981

Changes in intracellular pH regulation of skeletal muscle of rats with aortic stenosis.

Intracellular pH (pHi) of triceps, trapezius, quadriceps and gastrocnemius muscle tissue was determined in rats with myocardial hypertrophy due to experimental aortic stenosis (AS) and in sham operated rats (SO). During normocapnia, no significant difference in pHi between AS and So animals was observed in any of the muscle species investigated. In hypercapnia (FICO2 0.06, 0.075 or 0.100) pHi of AS was significantly higher than pHi of SO in all muscles, despite no difference in pHe, PaCO2 or [HCO3]a between AS and SO. Therefore, AS appears to be associated with an improvement of pHi regulation in skeletal muscle. In this respect, skeletal muscle behaves as hypertrophic cardiac muscle, which also shows an increased ability to regulate pHi in AS. These results suggest that the changes in pHi regulation of hypertrophic myocardium are not due to the hypertrophic process per se, but to a general phenomenon secondary to AS.

Acid-Base Equilibrium↗
PubMed1981

Myocardial intracellular pH regulation during chloride depletion.

The possible role of a HCO-3/Cl- transmembrane exchange as a mechanism of alkalinization in the myocardial cell was studied in isolated rabbit hearts perfused with Ringer solution. Cl- depletion was produced by replacing Cl- of the perfusate by SO2(-4) or glucuronate. Intracellular pH (pHi) was calculated both in Cl--free and Cl--containing hearts from the distribution of 14C-labeled 5',5'-dimethyloxazolidine-2,4-dione. Acid-base alterations were produced by changing perfusate HCO-3 concentration and/or CO2 partial pressure (PCO2). Depletion of Cl- resulted in an increase in pHi for any given level of extracellular pH. Increasing PCO2 at constant perfusate HCO-3 resulted in changes in pHi and cell HCO-3 (HCO-3i) that were similar in both Cl--free and Cl--containing hearts. Increasing perfusate HCO-3 at constant PCO2 resulted in increases in pHi and HCO-3i in both Cl--free and Cl--containing preparations. When the increases in HCO-3i secondary to an increase in extracellular HCO-3 were plotted as a function of the initial HCO-3i, a significant negative correlation was observed, suggesting that the elevation of HCO-3i was influenced by the initial HCo-3i and not by the presence or absence of Cl-. It is concluded that even though HCO-3 may enter the myocardial cells in exchange for Cl- during Cl-depletion, lack of Cl- does not alter the ability of the myocardial cell to regulate its pHi. This argues against a HCO-3/Cl- exchange as a mechanism of regulation of myocardial pHi.

Acid-Base Equilibrium↗
PubMed1979

Intracellular pH regulation of normal and hypertrophic rat myocardium.

The myocardial cell pH (pHi) observed during breathing of 0, 7.5, or 10% CO2 in air for 3 h was studied in rats with myocardial hypertrophy due to aortic stenosis and in sham-operated rats. The change in pHi during hypercapnia was significantly smaller in the rats with myocardial hypertrophy, with the apparent nonbicarbonate buffer value (delta [HCO3-]i/delta pHi) being almost three times that of the sham-operated rats. In vitro CO2 equilibrium of myocardial tissue homogenates showed no difference in nonbicarbonate buffer value between homogenates obtained from normal rats and from rats with myocardial hypertrophy. Therefore, it appears that the increased ability of the myocardial cell to regulate its pH during hypertrophy is not due to an increase in the cellular level of nonbicarbonate buffers, but seems to be related to a larger bicarbonate uptake by the myocardial cell during hypercapnia.

Acid-Base Equilibrium↗
PubMed1978

The effect of dibutyryl cyclic AMP and glucagon on the myocardial cell pH1.

DBcAMP or crystalline glucagon was utilized to elevate the intracellular cyclic AMP concentration in isolated rat hearts. Butyric acid, a metabolite of DBcAMP, was also investigated. Their effect on the intracellular pH (pHi) as determined by the distribution of [14C]DMO was investigated. Rat hearts, perfused with a recirculated modified Krebs-Henseleit solution maintained at 30 degrees C, were exposed to respiratory acidosis by bubbling the perfusate with 20% CO2. alpha- and beta-receptor antagonists were used to block the effects of endogenous catecholamines. Hypercapnia decreased the pHi from 7.09 to 6.82. A similar degree of hypercapnia decreased the pHi to only 6.95 in the presence of DBcAMP and to only 6.96 in the presence of glucagon. The effective buffer values (delta[HCO-3]i/deltapHi) were: control, 19; butyric acid, 16; DBcAMP, 139; glucagon, 148. These data suggest that cAMP mediates the effect of norepinephrine, which has been shown to diminish the change in pHi accompanying respiratory acidosis.

Acid-Base Equilibrium↗
PubMed1977

Determinants of transmembrane bicarbonate flux during acid-base changes.

Experiments were designed to determine the contribution of increased extracellular HCO3- concentration, [HCO-3e], to the net extracellular-to-intracellular HCO3- flux observed in hearts during hypercapnia. Isolated rabbit hearts were perfused by recirculating for 15-min periods a small volume of Ringer solution in which [HCO-3e] and carbon dioxide tension (PCO2) could be independently altered. A net HCO-3 flux was evidenced by a decrease in [HCO-3e] during recirculation. [HCO-3e] was randomly increased from 19 mM over a range of 19-42 mM at a constant PCO2 of 38.7 Torr. The resulting flux increased linearly with the [HCO-3e] existing at the start of recirculation. The same relationship was observed at 95.8 Torr PCO2. The disappearance of HCO-3 from the perfusate could not be explained by dilution in the interstitium or by lactate accumulation. When PCO2 was increased from 40 Torr over a range of 40-160 Torr at a constant [HCO-3e] of 20 or 30 mM, a small flux was observed only at the highest PCO2 levels. Essentially the same results were obtained when recirculation time was prolonged to 30 min. These results suggest that the major determinant of the HCO-3 flux is a change in extracellular HCO-3 concentration.

Acid-Base Equilibrium↗
PubMed1977

Contribution of a net transmembrane HCO3- flux to intracellular acid-base regulation.

Experiments were performed to determine the relative effects of a net extracellular-to-intracellular HCO3- flux and of elevated carbon dioxide tension (PCO2) on cellular acid-base regulation. Isolated rabbit hearts were perfused by recirculating a small volume of Ringer solution in which the PCO2 and the HCO3- concentration could be independently altered. Net HCO3- flux was assessed by the disappearance of HCO3- from perfusate. Between 40 and 100 Torr PCO2, a HCO3- flux into the cell occurs only when perfusate HCO3- concentration is increased. Therefore, by selective manipulation of perfusate HCO3- and PCO2 it is possible to induce hypercapnia with or without an accompanying HCO3- flux. When perfusate HCO3- concentration was increased from 20 to 36 mM, cellular HCO3- concentration increased from 22.5 +/- 0.8 to 26.1 +/- 1.0 mM at 40 Torr PCO2 and from 27.8 +/- 0.7 to 34.1 +/- 1.4 mM at 98 Torr PCO2. These increases can be accounted for by the amount of HCO3- that disappeared from the perfusate. The results suggest that most of the initial cell CO2 buffering is provided by the net HCO3- flux in addition to the passive physicochemical buffering.

Acid-Base Equilibrium↗
PubMed1976

Cardiac and skeletal muscle acid-base composition during metabolic acidosis in dogs.

Nephrectomized, open chested dogs were infused with 25-30 ml.kg(-1) body weight of 0.15 M NaCl (group I), 0.15 MHCl (Group II) or 0.3 M lactic acid (Group) III). Pulmonary ventilation was maintained constant in the three groups. Intracellular pH was calculated with the CO2 method. No significant intracellular or extracellular acid-base changes were produced in Group I. A similar degree of extracellular acidosis was achieved in Groups II and III. In spite of constant arterial PCO2, the PCO2 of mixed, coronary sinus and femoral vanous blood increased moderately after the infusion in Groups II and III. It was calculated that less than half of the HCl acid infused remained in the extracellular space. However, no significant changes were observed in the acid-base composition of skeletal muscle in either Group II or III. Comparison of the cardiac muscle cell acid-base composition of Group I with that of Groups II and III whows that metabolic acidosis of the degree and duration produced in these experiments does not produce appreciable myocardial acidosis.

Acid-Base Equilibrium↗
PubMed1976

Changes in skeletal muscle cell pH during graded changes in PCO2.

Blood perfusing isolated dog gracilis muscles was equilibrated with CO2 tensions ranging from 30 to 120 mm Hg, resulting in venous P CO2 from 35 to 135 mm Hg. Extracellular pH values ranged from 6.96 to 7.41, and muscle cell pH, calculated from DMO distribution, ranged from 6.64 to 6.94. When intracellular pH was plotted as a function of the corresponding extracellular pH, a linear relationship (r = 0.92) was observed throughout the entire pH range. The slope deltapHi/deltapHe was 0.64, without evidence of a difference in slope at different pH values. These results do not support the previous observations in rat diaphragms that cell pH is not affected by PCO2 changes over a certain extracellular pH range. pHe was 0.64, without evidence of a difference in slope at different pH values. Theses results do not support the previous observations in rat diaphragms that cell pH is not affected by PCO2 changes over a certain extracellular pH range.

Acid-Base Equilibrium↗
PubMed1976

Myocardial CO2 buffering: role of transmembrane transport of H+ or HCO3-ions.

Isolated rabbit hearts were perfused with rabbit red cells suspended in Ringer solution. A small volume of perfusate was recirculated for 10 min at Pco2 of 33.4 +/- 0.9 or 150.8 +/- 7.5 mmHg. Hypercapnia resulted in an increase in perfusate HCO3- concentration that was smaller than that observed when isolated perfusate was equilibrated in vitro with the same CO2 tensions (delta HCO-3e = 1.6 mM, P less than 0.01). This difference is consistent with a net movement of HCO3- into or H+ out of the mycardial cell, and cannot be accounted for by dilution of HCO3- in the myocardial interstitium. Recirculation of perfusate through the coronary circulation at normal Pco2 for two consecutive 10-min periods was not followed by changes in perfusate HCO3- concentration. A high degree of correlation (r = 0.81) was observed between intracellular HCO-3e concentration and the corresponding delta HCO-3e in individual experiments. The results suggest that transmembrane exchange of H+ or HCO3- is a buffer mechanism for CO2 in the myocardial cell.

Animals↗
PubMed1976

Effect of beta-adrenoreceptor blockade on rat cardiac and skeletal muscle pH.

The effect of catecholamines on the intracellular pH of rat cardiac and skeletal muscle during varying extracellular acid-base states was determined. Intracellualr pH (pHi) was calculated from the distribution of [14C]DMO. Acid-base disturbances were produced by placing the animals in an environmental chamber containing 10 or 20% CO2 or by administering HCL or NaHCO3. Two hours later the animals were anesthetized with sodium pentobarbital and blood and tissue samples obtained. In one series of animals, the effects of catecholamines were attenuated by administering the beta-adrenoreceptor antagonist MJ 1999 (Sotalol). In animals breathing 20% CO2, cardiac muscle pH was lower in beta-blocked than unblocked animals (6.69 vs. 6.78). During metabolic acidosis, cardiac muscle pH of beta-blocked animals was lower than that of unblocked animals (6.75 vs. 6.84). The same relationship was observed for skeletal muscle during metabolic acidosis-beta blockade pHi, 6.66; unblocked pHi, 6.77. The pHi of beta-blocked versus unblocked animals was not significantly different under normal acid-base conditions or metabolic alkalosis for cardiac or skeletal muscle. The effective buffer value of both tissue over the normal acidotic range was decreased by the beta-blocking agent. These results indicate that catecholamine release accompanying acidosis attenuates the change in pHI and increases the effective buffer value of cardiac and skeletal muscle.

Acid-Base Imbalance↗
PubMed1975

Inotropic and intracellular acid-base changes during metabolic acidosis.

Experiments in isolated, Ringer-perfused isovolumic rabbit hearts showed that metabolic acidosis resulted in a decrease in peak left ventricular pressure and dP/dt. Concomitantly, the decrease in extracellular pH from 7.28 plus or minus 0.02 to 6.82 plus or minus 0.02 at constant PaCO2 was associated with a negative av HCO3- difference that lasted throughout the duration of acidosis. This negative av HCO3- difference indicated that either HCO3- moved into the intravascular space or H+ moved in the opposite direction during acidosis. During perfusion with normal pH solution av HCO3- was not significantly different from zero. Washout of the extracellular space with the acid solution can account for only 32 percent of the total amount of HCO3-recovered in the venous perfusate during the 30 min of acidosis. The remaining 68 percent (10.7 plus or minus 3.1 mmol times kg-1 of cardiac tissue) must then have originated in the cellular fluid. When intracellular fluid volume is taken into account, it can be calculated that 21.3 plus or minus 6.1 mmol of HCO3- moved into the vascular space per liter of intracellular water. The magnitude of this HCO3- flux suggests that significant myocardial cellular acid-base changes are associated with metabolic acidosis.

Acidosis↗