Renal function during arterial hypertension produced by chronic splanchnic nerve stimulation in the dog.

نویسندگان

  • W G KUBICEK
  • F J KOTTKE
  • D J LAKER
  • M B VISSCHER
چکیده

Trained conscious mongrel dogs were used as the experimental animals. Arterial blood pressure was measured by means of a van Leersum carotid loop (3, 4). Renal plasma flow (RPF) and glomerular filtratration (GF) were determined by para-aminohippurate (PAH) and creatinine clearances, respectively. Filtration fraction (FF) was calculated from RPF and GF. Creatinine and PAH were administered intravenously by a constant-injection pump. Dosage was based on the surface area of the dog which was calculated by the Meeh-Rubner formula: surface area (M2) = I I ,z W-~7/IOo (W = weight in kg, M = meters). Priming dosages were : PAH, 385 mg/M2; creatinine, 1530 mg/M2. Sustaining dosages were: PAH, 5.75 mg/M2/min. ; creatinine, I 2 mg/M2/min. Plasma PAH and creatinine concentrations were maintained as nearly as possible at 2 mg yO and 12 mg %, respectively. Aft er a 2o-minute period for equilibration, urine samples were collected every 20 minutes by catheter and the bladder was flushed with three 30-cc aliquots of normal saline. Jugular vein blood samples were taken at the midpoint of the period. Plasma PAH determinations were made by the Bratton and Marshall method (5) as modified by Smith et al. (6), and plasma creatinine by the method of Folin and Wu (7). All clearances were performed on animals fasted approximately 18 hours. Five-hundred ml of water were given via stomach tube about 30 minutes before starting the clearance procedures. Renal plasma flow in cubic centimeters/minute/square meter was calculated from: RPF = C,V,/.go Cp TA, in which C, = (urine plus wash) concentration of PAH; V, = urine volume plus wash dilution (ml) ;

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Cardiovascular responses to hypothalamic arcuate nucleus stimulation in the rat: role of sympathetic and vagal efferents.

Experiments were carried out in urethane-anesthetized, artificially ventilated, adult male Wistar rats. Microinjections (50 nL) of N-methyl-d-aspartic acid (1, 5, and 10 mmol/L), but not artificial cerebrospinal fluid, into the hypothalamic arcuate nucleus (ARCN) elicited increases in mean arterial pressure (5.7+/-0.5, 13.2+/-1.4, and 17.3+/-1.1 mm Hg, respectively) and heart rate (24.3+/-4.3, ...

متن کامل

Splanchnic circulation is a critical neural target in angiotensin II salt hypertension in rats.

Chronic angiotensin II (Ang II) infusion, in rats fed high salt, engages the sympathetic nervous system to increase venomotor tone. The splanchnic sympathetic nervous system is the most important regulator of venous tone, indicating that splanchnic sympathetic nervous system activity may be increased in Ang II salt hypertension. We hypothesized that celiac ganglionectomy (CGx), to selectively d...

متن کامل

Continuous angiotensin II blockade throughout the acute phase of one-kidney hypertension in the dog.

The importance of the renin-angiotensin system in the development and maintenance of one-kidney renal hypertension in the dog was assessed by chronically inhibiting angiotensin by continuous infusion of [Sar'-,Ala]angiotensin II or a converting enzyme inhibitor (SQ 20881). Angiotensin blockade was begun 1-2 days before renal artery constriction and continued for 6-7 days throughout the high rer...

متن کامل

Dietary salt intake exaggerates sympathetic reflexes and increases blood pressure variability in normotensive rats.

Previous studies have reported that chronic increases in dietary salt intake enhance sympathetic nerve activity and arterial blood pressure (ABP) responses evoked from brain stem nuclei of normotensive, salt-resistant rats. The purpose of the present study was to determine whether this sensitization results in exaggerated sympathetic nerve activity and ABP responses during activation of various...

متن کامل

The production of arterial hypertension by chronic renal artery-nerve stimulation.

Since reducing the blood flow to the kidneys by mechanical constriction of the renal arteries produces hypertension (2, 4, 6, 14), it seemed desirable to ascertain whether decreasing renal blood flow by sfimulation of renal vasocon-strictor nerves might likewise cause an elevation in blood pressure. It is known (3, 7, 10, 15) that active renal vasoconstriction occurs in response to stimulation ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • The American journal of physiology

دوره 174 3  شماره 

صفحات  -

تاریخ انتشار 1953