RESUMEN
Albino rats were made hypertensive by 1% NaCl in the drinking water for 4-5 months, systolic (SBP) and distolic blood pressure (DBP) were 164.0 +/- 10.1 mm Hg and 118.7 +/- 4.6 mm Hg respectively, vs. control rats whose SBP and DBP were 119.0 +/- 4.4 mm Hg and 86.8 +/- 4.3 mm Hg respectively. Psychosocial stress (1 hour daily for 4-5 months) only raised SBP to 140.0 +/- 5.2 mm Hg; DBP remained unaltered. One percent NaCl intake combined with psychosocial stress, increased SBP and DBP but not significantly beyond the level observed with single 1% NaCl administration. Formerly described control and hypertensive rats were anesthetized with sodium pentobarbital (40 mg/kg) and stereotaxically injected into de cisterna magna (i.c.) with 20 microliters of 1.5 M NaCl solution. During i.c. injection, intraarterial SBP, DBP and heart rate (HR) were continuously recorded. After i.c., 1.5 M NaCl injection, mean arterial pressure (MAP) increased 21.0 +/- 4.0 mm Hg and HR 51.0 +/- 5.0 beats/min in control rats. Rats made hypertensive by 1% NaCl intake showed a significantly lower increase of MAP, 11.0 +/- 1.8 mm Hg; HR increased 37.0 +/- 4.3 beats/min. Rats submitted only to psychosocial stress displayed a response similar to the one described in control rats. Hypertensive rats submitted to both 1% NaCl intake and psychosocial stress had a more intense reduction of the hypertensive and tachycardic response, 8.0 +/- 2.2 mm Hg and 20.0 +/- 3.2 beats/min respectively. Control i.c. injection with the same volume of saline (0.15 M NaCl) did not change significantly SBP, DBP or HR in a separate group of rats. Left ventricle weight (0.754 +/- 0.0333 g) was augmented in the 1% NaCl treated group (0.795 +/- 0.038 g), and increased its protein content by 13.1% (changes not statistically significant). The highest increase of the left ventricle weight (23.7% above control) with no change in its protein content was observed in rats submitted to 1% NaCl intake plus psychosocial stress. In conclusion, chronic high NaCl intake increased blood pressure; psychosocial stress acted as a weak stimulus for SBP and DBP increase, and central nervous system sodium chloride sensitivity for delivering a peripheral sympathetic discharge was found decreased in rats made hypertensive by a high salt intake.
Asunto(s)
Presión Sanguínea/efectos de los fármacos , Sistema Nervioso Central/efectos de los fármacos , Cisterna Magna , Frecuencia Cardíaca/efectos de los fármacos , Hipertensión/fisiopatología , Cloruro de Sodio/farmacología , Animales , Diástole/efectos de los fármacos , Masculino , Tamaño de los Órganos/efectos de los fármacos , Proteínas/análisis , Proteínas/efectos de los fármacos , Ratas , Ratas Sprague-Dawley , Estrés Psicológico/inducido químicamente , Sístole/efectos de los fármacosRESUMEN
Dopamine is synthetized and excreted by kidneys, this amine exerts its natriuretic and diuretic effects by inhibition of sodium reabsorption on kidney convoluted tubules. The objective of this study was to verify the changes of dopamine urinary excretion induced by nifedipine-LP treatment in hypertensive patients. Twenty four patients with essential hypertension (stages 1, 2) were included in this double-blind, placebo controlled study. Twelve patients received nifedipine (average daily dose, 21.5 mg/day) for 4 weeks, and 12 patients received placebo for the same time period. No significant changes were detected upon nifedipine treatment neither in plasma biochemical nor hematological parameters. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) was significantly reduced from pretreatment values 168.0 +/- 8.7 mmHg and 102.0 +/- 5.2 mmHg respectively, to end-treatment values 140.0 +/- 6.6 mmHg and 88.0 +/- 5.6 mmHg (p < 0.05). Placebo treatment did not modify SBP and DBP. Urinary dopamine excretion increased by 53% from 679.5 +/- 80.1 micrograms/24 h prior to treatment to 1040.0 +/- 110.1 micrograms/24 h after treatment (p < 0.009. 95% Confidence Interval of the Difference: -538.9 to -183.6). Urinary volume of nifedipine treated patients increased from 1613 +/- 85 mL/24 h to 1920 +/- 160 mL/24 h post-treatment (p < 0.05). No significant changes were observed in urinary noradrenaline and adrenaline excretion in nifedipine or placebo treated patients. Analysis of fluorescent light excitation and emission spectra (200 nm to 800 nm) of dopamine extracted from patient's urine submitted to nifedipine treatment did not reveal any interference when compared to chemically pure dopamine. If is concluded that nifedipine treatment of hypertensive patients increases kidney dopamine production which in turn can exert a natriuretic and diuretic effect besides its well known vasodilator properties.