The adrenal renal vascular connection plays an essential role in the pathogenesis of renovascular hypertension in the rat.

The adrenal renal portal circulation (ARPC) contributes to decrease in renal blood flow occurring after renal artery clipping. The aim of present study was to determine the role of the ARPC in the development of the renovascular hypertension in 1-kidney 1-clip model in the rat. Experiments were performed on male Wistar rats. In the control group (A) the right nephrectomy and adrenalectomy were done. In the experimental groups renovascular hypertension was produced by clipping the left renal artery (silver clip ID 0.40 mm). In the first of the experimental groups (B) the right nephrectomy and adrenalectomy were done. In the second experimental group (C), for elimination of the ARPC, the right kidney and the left adrenal gland were removed. In the half number of rats from each group plasma renin activity was measured 48 hours after surgery. An increase in SBP was significantly higher in the group B (ARPC intact) than in the group C (ARPC eliminated) (172 +/- 4 vs 144 +/- 2 mmHg, p.<0.01). PRA was significantly higher in the group C than in the group B (39.0 +/- 1.4 vs 31.2 +/- 2.0 mmol/l/min, p.<0.05). In the control group (A) PRA was significantly lower as compared to the both experimental group (2.0 +/- 1.6 mmol/l/min, p.<0.05).

[A case of a case of mild cognitive impairment--diagnostic uncertainties]. / Przypadek lagodnych zaburzen funkcji poznawczych--watpliwosci diagnostyczne.

In the paper a case of mild cognitive impairment is presented. It is interesting because of its atypical psychopathological picture. The primary disorder is accompanied with symptoms of depression and anxiety. A course of diagnosis and treatment are outlined.

Arterial hypertension due to occlusion of the adrenal vein in the rat is strain-dependent.

OBJECTIVE: To determine whether the development of arterial hypertension due to occlusion of the central adrenal vein in the rat is strain-dependent DESIGN AND METHODS: The experiments were performed on male rats weighing 300-400 g each, of the following strains: Wistar outbred, Wistar Glaxo, Lewis, Wistar-Kyoto (WKY) rats bred for high blood pressure (138 +/- 13.2 mmHg), WKY rats bred without the control of blood pressure (118 +/- 12.9 mmHg) and borderline hypertensive rats (BHR). BHR were the F1 spontaneously hypertensive rat and WKY rat crossbred rats. In order to increase blood flow through the adrenal-renal portal circulation, both central adrenal veins of rats in the experimental group were occluded. The systolic blood pressure was measured indirectly by a photoelectric method. RESULTS: By the ninth day after surgery systolic blood pressure had increased significantly only in the WKY rats bred for high blood pressure and BHR, reaching maximal values on 12th day for WKY rats bred for high blood pressure (167 +/- 5 mmHg) and on the 18th day for BHR (170 +/- 14 mmHg). CONCLUSIONS: These data show that the development of arterial hypertension due to augmentation of adrenal blood flow through adrenal-renal portal circulation occurs in rats of strains with a genetic background of hypertension.

Occlusion of the adrenal vein leads to an increase in renal vascular resistance in the ipsilateral kidney.

1. The aim of the present study was to investigate the effect of an acute increase in blood flow through the adrenal-renal vascular connection (ARVC), due to occlusion of the adrenal vein, on renal blood flow (RBF) and renal vascular resistance (RVR). 2. Experiments were performed in Wistar-Kyoto rats. Animals were divided into four groups. In the first group, the adrenal vein was clamped using a metal clip. In the second group, the tissue between the adrenal gland and the kidney was cut before clamping. In the third and fourth groups, alpha-adrenoceptor blockade was induced by intravenous infusion of phentolamine before clamping the adrenal vein. In addition, in the fourth group, tissue between the adrenal gland and the kidney was cut before clamping. 3. In the first group, occlusion of the adrenal vein caused an increase in RVR, followed by a decrease in RBF. In the second, third and fourth groups, the same procedure did not change either RBF or RVR. 4. We conclude that the augmented inflow of catecholamines to the kidney through the ARVC changes the haemodynamics of the kidney and may contribute to development of arterial hypertension due to occlusion of the adrenal vein.

Adrenal-renal portal circulation contributes to decrease in renal blood flow after renal artery stenosis in rats.

The aim of the present study was to investigate a role of adrenal-renal portal circulation (ARPC) in a decrease in renal blood flow due to acute stenosis of the renal artery in rats. Animals were divided into three groups. In the control group (I), in order to eliminate the ARPC tissue between the adrenal gland and the ipsilateral kidney was cut. In the second and the third group (II) (III), left renal artery was stenosed by a silver clip (ID 0.40 mm). Then, in the group II, ARPC was surgically eliminated. In the group II, prior to the elimination of ARPC, alpha-adrenergic receptors blockade was produced by phentolamine administration. In the control group, ARPC elimination did not influence either renal blood flow (RBF) or renal vascular resistance (RVR). In the group II, elimination of ARPC caused increase in RBF and decrease in RVR In the group III elimination of ARPC influenced neither RBF nor renal vascular resistance (RVR). Results of the present study provide the functional evidence that catecholamines reaching the kidney through ARPC, contribute to the decrease in RBF and increase in RVR during acute renal artery stenosis in the rat.

The adrenal-renal vascular connection contributes to increase in renal vascular resistance during an experimental hypotension in the rat.

The adrenal vascular connection (ARVC) was described for the first time in the cat by Cow (1914) and by other authors in the dog, rat, rabbit and humans. The aim of the present study is to investigate the role of above connection in regulation of renal vascular resistance (RVR), and renal blood flow (RBF) during decrease in blood pressure in the rat. Animals were divided into three groups. In the first group, mean arterial pressure (MAP) was unchanged. In the second and the third group MAP was maintained at 50 mmHg. In addition in the third group, an alpha adrenergic receptor blockade was produced with intravenous infusion of phentolamine. After stabilisation of RBF, in all groups, the tissue between the adrenal gland and the kidney was cut. RBF and MAP were measured and recorded. In the first and the third group, the elimination of ARVC neither influenced RBF nor RVR. In the second group the elimination of ARVC caused increase in RBF and decrease in RVR (p < 0.01). Results of the present study provide the evidence that catecholamines reaching the kidney, directly from the adrenal gland through ARVC, during the severe hypotension are responsible for reducing of renal blood flow and increase in renal vascular resistance in the rat.

The increased concentration of 2,3-diphosphoglycerate in red blood cells of spontaneously hypertensive rats.

It has been recognised that high haemoglobin oxygen capacity is essential for the development of high blood pressure in spontaneously hypertensive rats. In the present study we have found increased concentration of 2,3 diphosphoglycerate (2,3-DPG) in red blood cells of spontaneously hypertensive rats (SHR) of Okamoto-Aoki strain. As 2,3-DPG is the major factor decreasing haemoglobin affinity to oxygen, our finding suggests that at given value of pO2 oxygen delivery to the tissue of SHR would be increased. Therefore increased concentration of 2,3-DPG in red blood cells of SHR would be of the pathophysiological meaning by promoting autoregulatory increase in total vascular resistance in this strain of rats. The mechanism responsible for enhanced synthesis of 2,3-DPG in SHR remains unclear. Intracellular alkalosis due to either hypocapnia and/or an enhanced activity of Na+/H+ antiporter occurring in SHR are the most plausible explanations for the above finding.

High renin arterial hypertension due to occlusion of the adrenal veins in the rat.

The direct adreno-renal vascular connection allows precise control of the kidney function by hormones produced by the adrenal gland, without any significant changes in their content in the whole blood. The purpose of the present study is to investigate the effect of the increased blood flow through the vascular network on the blood pressure. In twelve Wistar rats the central adrenal veins were ligated bilaterally. This procedure resulted in chronic increase in systolic blood pressure. This model of arterial hypertension is characterized by high plasma renin activity and normal aldosterone plasma concentration.