Hypokalaemia and respiratory acidosis following partial obstruction of the airway.

An 87-year-old female, with a history of hypertension controlled with hydrochlorothiazide, was scheduled for excision of a cystic mass of the left lobe of the thyroid. In the course of the anaesthetic, she developed partial airway obstruction that resulted in respiratory acidosis (PaCO2 108 mmHg, pH 7.06), developed premature ventricular contractions and experienced a reduction in plasma potassium concentration from 3.9 to 2.9 mmole X L-1. We interpret this hypokalaemia as a consequence of the epinephrine discharge due to hypercapnia. The case is reported to emphasize the importance of minimizing the sympathetic response to induction of anaesthesia, intubation and surgery in patients with marginal potassium stores.

Sympathetic control of renin release.

Sympathetic outflow influences the renal release of renin through modifications of the tonic activity of the renal nerves and the plasma concentration of catecholamines. These influences may initiate changes in the rate of renin secretion or modulate the response initiated by another of the mechanisms that control renin release. Beta-adrenoceptor mediated stimulation of renin release has been demonstrated in vivo, in the isolated perfused kidney and in preparation in vitro. Likewise an array of evidence has accumulated pointing to the existence of alpha-adrenoceptor mediated inhibition of renin release. However, the cellular location, the physiological significance, and even the existence of these alpha-adrenoceptors is still disputed. Receptors sensitive to alterations in the vascular volume have been identified in areas of low and high pressure of the circulation. There is evidence that input from both types of receptors may cancel each other, and that to demonstrate experimentally the effects on renin release of the low pressure cardiopulmonary receptors it is necessary to avoid changes in the input from the high pressure arterial receptors, and vice versa. Again there are dissenting voices that disclaim a tonic inhibitory effect of cardiopulmonary receptor initiated impulses on renin release. The majority of the pharmacological evidence identifies the beta-adrenoceptors in JG cells as of the beta 1-subtype. However, some species may make exception to this generalization. As in other tissues, beta-adrenoceptor mediated influences appear to relate to activation of adenylcyclase in the cell membrane. Considerable interest in the role of calcium in the process of activation of renin release has met with some unexpected, though consistent, experimental findings.

Effect of haemorrhage on renin concentration in superficial and deep venous outflows of the cat kidney.

1. Plasma renin concentration is significantly higher in the subcapsular venous outflow, which drains the superficial cortex, than in the deep venous outflow, which drains the inner half of the cortex and medulla of the cat kidney. The purpose of these experiments was to observe whether this pattern is preserved or disrupted by a stimulus to renin release. 2. Plasma renin concentration in arterial samples and in the superficial and deep renal venous outflows was measured before and after haemorrhage which produced a 24 +/- 6.7% drop in mean blood pressure in 13 cats. 3. After haemorrhage, total kidney plasma flow and glomerular filtration rate (GFR) did not change significantly. There was a rise in arterial plasma renin concentration. Venous minus arterial plasma renin concentration increased significantly in the deep venous outflow, but not in the superficial outflow. 4. The results suggest that both superficial and deep cortical venous drainage of the cat kidney should be considered when measuring renal renin release. In addition, they suggest that there may be differences in the response of superficial and deep juxtaglomerular apparatuses to haemorrhage.

Regional renin release by the cat kidney in vitro and in vivo.

Differences in the rate of renin release by superficial and deep areas of the cat kidney cortex were studied in vitro and in vivo. Renin release in vitro by outer cortical slices was significantly higher than by their inner counterparts: 19.6 +/- 2.3 vs. 12.8 +/- 1.95 ng angiotensin I-h-1-mg fresh tissue-1-h of incubation-1. In vivo blood was sampled from subcapsular (outer cortical) and deep (inner cortical and medullary) renal venous circulation from anesthetized cats. Renal venous minus arterial plasma renin concentration was respectively, 4.3 +/- 1.12 and 1.9 +/- 1.04 ng angiotensin I-ml-1-h-1 (P less than 0.01). By assuming that in these experiments renal blood flow distribution was approximately equal to each of the two areas of venous drainage, as reported in the isolated perfused cat kidney, we infer from the regional differences in arteriovenous concentration that the rate of renin release of the outer cortex is higher than that of the innder cortex in the cat kidney in vivo. Tissue content of renin was found to decrease toward the deep cortex. The results support the concept that the rate of regional renin release correlates with tissue renin content, at least under the conditions of the present experiments.

Relation between Na-K-ATPase activity and respiratory rate in the rat kidney.

The relation between Na-k-ATPase activity in homogenates of rat kidney and oxygen consumption in kidney slices was studied by employing different physiological maneuvers known to change the activity of renal Na-K-ATPase. Treatment of euthyroid rats with 3,5,3'-triiodo-1-thyronine increased Na-K-ATPase activity, sodium-dependent oxygen consumption (QO2[t]), and para-aminohippurate (PAH) accumulation by kidney slices without changing glomerular filtration rate or net sodium reabsorption by the intact kidney. Treatment with methylprednisolone also increased Na-K-ATPase, QO2[t], and PAH transport. Chronic potassium loading, on the other hand, increased renal Na-K-ATPase to the same degree as the first two procedures, but QO2[t] and PAH accumulation were unchanged. Partial nephrectomy induced an increase in the activity of Na-K-ATPase in homogenates of the remaining kidney fragment, but QO2[t] did not change significantly and PAH uptake was unaltered. An increase in the activity of Na-K-ATPase in kidney homogenates is therefore not necessarily associated with a parallel change in oxygen consumption by the intact cell.

On the mechanism of lithium-induced diabetes insipidus in man and the rat.

The mechanism of lithium-induced diabetes insipidus was investigated in 96 patients and in a rat model. Polydipsia was reported by 40% and polyuria (more than 3 liter/day) by 12% of patients receiving lithium. Maximum concentrating ability after dehydration and vasopressin was markedly impaired in 10 polyuric patients and was reduced in 7 of 10 nonpolyuric patients studied before and during lithium therapy. Severe polyuria (more than 6 liter/day) was unresponsive to trials of vasopressin and chlorpropamide, but improved on chlorothiazide. Rats receiving lithium (3-4 meq/kg/day) developed massive polyuria that was resistant to vasopressin, in comparison to rats with comparable polyuria induced by drinking glucose. Analysis of renal tissue in rats with lithium polyuria showed progressive increase in the concentration of lithium from cortex to papilla with a 2.9-fold corticopapillary gradient for lithium. The normal corticopapillary gradient for sodium was not reduced by lithium treatment. The polyuria was not interrupted by brief intravenous doses of vasopressin (5-10 mU/kg) or dibutyryl cyclic AMP (10-15 mg/kg) capable of reversing water diuresis in normal and hypothalamic diabetes insipidus rats (Brattleboro strain). The present studies suggest that nephrogenic diabetes insipidus is a common finding after lithium treatment and results in part from interference with the mediation of vasopressin at a step distal to the formation of 3',5' cyclic AMP.

The distribution of sodium-potassium--activated adenosine triphosphatase in medulla and cortex of the kidney.

The activity of sodium-potassium-activated adenosine triphosphatase (Na-K-ATPase) is considerably higher in homogenates of outer medulla than in the cortex or papilla of the kidney. The enzyme has similar kinetic characteristics in both cortex and medulla, and binds ouabain in the same proportion. The discrepancy in enzymatic activity is not paralleled by similar change in the activity of adenyl cyclase, 5'nucleotidase, glucose-6-phosphatase, or succinic dehydrogenase. Na-K-ATPase is also higher in distal convoluted tubules (ventral slices) than in the proximal tubules (dorsal slices) of the kidney of Amphiuma. The high concentration of Na-K-ATPase in the red medulla of the kidney is probably related to the presence here of the thick ascending limb of the loop of Henle, and this has important implications with regard to the mechanism of sodium reabsorption by different portions of the nephron.