The effects of antidiuretic hormone and state of potassium balance on the renin‐angiotensin system in rats with diabetes insipidus.

Fernández-Repollet, Emma; Maldonado, Manuel Martinez; Opava-Stitzer, Susan C.

doi:10.1113/jphysiol.1982.sp014089

Cited by 6 publications

(2 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Major alterations in the renin-angiotensin system are also prevalent [4] and include increased plasma ANG concentrations [18] and de creased angiotensin-converting enzyme activity in the ante rior pituitary gland [1,2).…”

Section: Discussionmentioning

confidence: 99%

Increased Number of Angiotensin II Binding Sites Determined by Autoradiography in Anterior Pituitary of Water-Deprived and Brattleboro Rats

Israel¹,

Plunkett²,

Saavedra³

1986

Neuroendocrinology

View full text Add to dashboard Cite

Pituitary angiotensin II (ANG) binding sites were characterized by autoradiography in individual male Long Evans (LE) rats, heterozygous Brattleboro (HZ) rats, and homozygous Brattleboro (DI) rats which were water satiated or water deprived. An additional group of DI rats was treated with arginine vasopressin for 1 week. The technique utilized 8-µm pituitary sections which were incubated with ¹²⁵I-[Sar¹]-ANG in concentrations ranging from 25 pM to 10 nM. Angiotensin binding in the anterior pituitary of water-satiated LE rats was characterized by a single class of high-affinity, saturable sites with a B_max of 1.309 ±119 fmol/mg of protein and a K_a of 0.51 ± 0.03 × 10⁹M^–1l. Compared to LE rats the density of ANG-binding sites in anterior pituitary was higher in DI rats (+84.2%), with HZ having an intermediate concentration (+41.6). Dehydration increased the ANG-binding site density in all groups. Five days of water deprivation increased the number of ANG-binding sites by 86.5% and by 36.9% in LE and HZ rats, respectively, when compared to their water-satiated controls. After 1 day of water deprivation, the ANG-binding site density increased by 19.4% in DI rats. No changes in ANG-binding sites occurred after hormonal replacement with arginine vasopressin in water-satiated DI rats. The binding affinity constant of the agonist for the ANG-binding sites compared with LE rats was decreased in both HZ and DI rats (-27.5 and -19.4%) and was also decreased after 5 days of dehydration in LE rats (-34%) when compared to the water-satiated state. Our results demonstrate alterations in ANG-binding sites in the anterior pituitary gland of both dehydrated Brattleboro rats and LE rats. These findings suggest a role for anterior pituitary ANG receptors in the regulation of fluid metabolism in the rat.

show abstract

Section: Discussionmentioning

confidence: 99%

Increased Number of Angiotensin II Binding Sites Determined by Autoradiography in Anterior Pituitary of Water-Deprived and Brattleboro Rats

Israel¹,

Plunkett²,

Saavedra³

1986

Neuroendocrinology

View full text Add to dashboard Cite

show abstract

“…Because ADH plays a permissive role in enhancing K + excretion, a water diuresis due to a lack of ADH actions does not increase K + excretion appreciably [43]. Only an increased osmole excretion rate can drive more K + secretion in the CCD and this can be indirectly estimated by the ratio of the osmolality to Cr in the urine when a spot urine is analyzed [44].…”

Section: Urine Flow Ratementioning

confidence: 99%

Hypokalemia: A Practical Approach to Diagnosis and its Genetic Basis

Lin¹,

Halperin²

2007

CMC

View full text Add to dashboard Cite

Hypokalemia is a common and important finding in hospitalized patients because it may provoke cardiac arrhythmias and/or respiratory arrest. Our aim is to suggest better diagnostic tools and therapeutic principles, and summarize new molecular advances that are linked to hypokalemia. Measurements in freshly-voided urine to evaluate potassium (K+) excretion and an assessment of the acid-base status in blood can help differentiate between the various causes of hypokalemia. In patients with a low rate of K+ excretion, hypokalemia can be explained by an acute shift of K+ into cells, intestinal K+ loss, or prior renal K+ excretion. Patients with a high rate of K+ excretion usually have metabolic acid-base disorders. In patients with hyperchloremic metabolic acidosis, an assessment of the rate of excretion of ammonium (NH4+) in the urine separates those with renal tubular acidosis (RTA) (low NH4+ excretion) from those with causes other than RTA. In patients with metabolic alkalosis, a high blood pressure helps to distinguish between a state with high mineralocorticoid activity from others with extracellular fluid (ECF) volume contraction. Measurement of renin activity, aldosterone, and cortisol levels in plasma help to differentiate between the causes with mineralocorticoid excess whereas the urine chloride (Cl-) concentration may reveal the basis for renal Na+ wasting and distinguish it from non-renal Na+ loss. The treatment of hypokalemia is guided by the risk imposed by hypokalemia, magnitude of the K+ deficit, route of the K+ administration, available K+ preparations, adjuncts to therapy, and special associated conditions. Recent molecular advances in inherited hypokalemic disorders affecting transcellular K+ shift, gastrointestinal and renal K+ excretion are also discussed.

show abstract

Elevated glucose utilization in subfornical organ and pituitary neural lobe of the Brattleboro rat

et al. 1983

View full text Add to dashboard Cite

The effects of antidiuretic hormone and state of potassium balance on the renin‐angiotensin system in rats with diabetes insipidus.

Cited by 6 publications

References 25 publications

Increased Number of Angiotensin II Binding Sites Determined by Autoradiography in Anterior Pituitary of Water-Deprived and Brattleboro Rats

Increased Number of Angiotensin II Binding Sites Determined by Autoradiography in Anterior Pituitary of Water-Deprived and Brattleboro Rats

Hypokalemia: A Practical Approach to Diagnosis and its Genetic Basis

Elevated glucose utilization in subfornical organ and pituitary neural lobe of the Brattleboro rat

Contact Info

Product

Resources

About