Effect of central norepinephrine depletion on renovascular hypertension and on the renin system
| Autor: | Alberto C. Taquini, Maria Luisa Kurnjek, Patricia Ruiz, Nidia Basso |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
Male
medicine.medical_specialty Sympathetic Nervous System Physiology Angiotensinogen Blood Pressure Renovascular hypertension Norepinephrine (medication) Renin-Angiotensin System Norepinephrine Cerebrospinal fluid Internal medicine medicine.artery Renin–angiotensin system Renin Internal Medicine Medicine Animals Renal artery Rats Wistar Oxidopamine business.industry Sympathectomy Chemical Brain General Medicine medicine.disease Rats Endocrinology Blood pressure Hypertension Renovascular Hypothalamus Catecholamine business medicine.drug |
| Zdroj: | Clinical and experimental hypertension (New York, N.Y. : 1993). 15(4) |
| ISSN: | 1064-1963 |
| Popis: | Some reports have stated that central norepinephrine (NE) depletion inhibited the development of hypertension in the rat. On the other hand, this pharmacological treatment induces changes on the central renin-angiotensin system. The present study was designed to follow the development of 2 kidney-2 clip (2k-2c) renovascular hypertension in rats depleted of central NE and to analyze the central and peripheral renin-angiotensin system. Male Wistar rats (n = 40) were used. Half of the animals was injected, intracisternally, with 6-hydroxydopamine (6-OHDA), the remaining rats only received the vehicle. One week later a silver clip was placed on each renal artery on half of the 6-OHDA treated rats and on half of the vehicle treated animals. A sham operation was performed on the remaining rats. Blood pressure was measured weekly during 7 weeks. Then, blood and cerebrospinal fluid (CSF) samples were obtained. The brain was dissected in several areas. NE and angiotensinogen concentration (AoC) were determined in tissue samples. AoC was evaluated in plasma and CSF; plasma renin activity was also measured. Hypertension development was not prevented by central NE depletion, which was significant in all central areas (p0.001). Other significant results showed that renal ischemia and/or NE depletion induced a significant increase in angiotensinogen concentration in the hypothalamus (p0.01) and in CSF (p0.05). In summary: central NE depletion was not able to modify the development of 2 k - 2 c hypertension. Treatment and renal ischemia induced an increase of central AoC. |
| Databáze: | OpenAIRE |
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