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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The properties of artificial lipid membranes modified by frog offactory preparation obtained by ultrasonic treatment of frog olfactory tissues were investigated. Out of the 24 odorous substances which were tested five active stimulants were identified each inducing a resistance drop of the modified membrane when added to the cell. The studies of this effect in solutions with different salt content demonstrated that the decrease in resistance resulted most probably from an increased membrane permeability to Na+ ions. The dyes did not affect the resistance of modified membranes. Mercury bichloride at the concentration of 5 . 10(-4) M was shown to block the responce of the membrane when added to the cell prior to stimulants. At the same time mercury biochloride did not practically affect the membrane resistance after its response to the odorants. The possible ways of increasing the sensitivity of modified membranes to odorants are discussed.
Mol Biol (Mosk)
PMID:[Molecular basis of olfactory reception. I. Artificial lipid membrane sensitive to odorous substances]. 105 70

1. Oral administration of DL-alpha-tocopheryl nicotinate (EN) (0-04 or 0-2 mmol day-1 kg-1) or DL-alpha-tocopharyl acetate (EA) (0-2 mmol day-1 kh-1) delayed the progress of hypertension in unilaterally nephrectomized rats, which were treated with deoxycorticosterone and salt, and in genetically hypertensive rats (SHR) which were given sodium chloride solution. Suppression of body weight gain, incidence of pneumonia and mortality were reduced by treatment with EN or EA. 2. Severe hypertension in old SHR (9 months) further progressed, when drinking water was replaced by sodium chloride solution, and four out of ten of these animals died of cerebral haemorrhage during 4 weeks. The administration of EN or EA prevented the increase in blood pressure and incidence of stroke.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Anti-hypertensive action of DL-alpha-tocopharyl esters in rats. 107 97

1. Patients with end-stage renal disease and anephric patients underwent expansion and depletion of body fluids with salt and water. This resulted in four different sequential haemodynamic patterns: (i) no significant increase in blood pressure; (ii) increase in blood pressure associated with a rise in cardiac output and no effect on total peripheral resistance; (iii) increase in cardiac output followed by a rise in blood pressure and total peripheral resistance; (iv) increase in total peripheral resistance and blood pressure without significant changes in cardiac output. 2. It is concluded that an initial rise in cardiac output is not necessary to increase-blood pressure in either anephric man or patients with end-stage renaldisease.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The haemodynamic response to salt and water loading in patients with end-stage renal disease and anephric man. 107 13

1. The role of renal medullary prostaglandin E has been examined in rats with hypertension induced by sodium chloride and deoxycorticosterone (salt-DOC). 2. Synthesis of prostaglandin E was normal in early salt-DOC hypertension. Indomethacin exacerbated the hypertension, and depressed synthesis of prostaglandin E equally in hypertensive and control rats. 3. Synthesis of prostaglandin E was depressed in rats with late salt-DOC hypertension. 4. The results lend support to the concept that prostaglandin E is involved in the regulation of arterial pressure.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Renal prostaglandin synthesis in hypertension induced by deoxycorticosterone and sodium chloride in the rat. 107 21

1. Urinary kallikrein excreted by normal rats is significantly increased (P less than 0-001) 2 h after: (a) water loading, (b) water loading plus frusemide, 0-27 mmol (10 mg) per rat, (c) salt loading. In water-loaded rats, 5 i.u. of renin strikingly reduced kallikrein excretion (P less than 0-01) but considerably increased sodium excretion (P less than 0-001). 2. Renal kallikrein, measured by its kininogenase activity within 2 h of water loading, was significantly increased (P less than 0-05); after water loading and frusemide it was 40% decreased (P less than 0-001) and after salt loading it was reduced by approximately 50% (P less than 0-02). Renin did not change renal kallikrein. 3. Severely hypertensive (one-kidney) rats (blood pressure greater than 150 mmHg) showed no increase of urinary kallikrein after water loading, although there was a marked natriuresis, in moderately hypertensive rats (blood pressure less than 150 mmHg) urinary kallikrein was only one-third of that observed in control normotensive rats, after an equal degree of water loading.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Renal urinary kallikrein in normotensive and hypertensive rats during enhanced excretion of water and electrolytes. 107 23

1. The arteriolar lesions of rats with deoxycorticosterone (DOCA)-salt hypertension have been studied by colloidal carbon injection and light- and electron-microscopy. 2. Colloidal carbon particles enter the media of arterioles to form focal deposits when hypertension develops. 3. The focal lesions are similar to those seen after angiotensin infusion or renal artery constriction. They are characterized by endothelial damage and plasma deposition in the media. 4. Heavy deposition of carbon in the glomeruli of DOCA-treated animals was found to be caused by increased mesangial uptake and not by hypertensive vascular damage. 5. Angiotensin II concentrations fell during the development of hypertension and vascular lesions. The renin-angiotensin system was not implicated in the development of vascular damage in this form of hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The arteriolar lesions of steroid hypertension in rats. 107 33

1. Renal and cerebral vascular lesions occurred more often and earlier in spontaneously hypertensive rats (SHR) given a high salt diet than in SHR given a normal diet. 2. Kidney renin activity was low during high salt loading; the kidney renin activity of rats with hypertensive renal vascular lesions was moderately elevated. Kidney renin activity or cathepsin D activities were higher in stroke-prone SHR (SHRSP) aged 9 months than in stroke-resistant SHR (SHRSR). 3. beta-Glucuronidase, cathepsin D and deoxyribonuclease activities were greater in the kidney of Wistar/Kyoto (WK) rats or SHR when there were hypertensive vascular lesions. These three enzyme activities were also greater in the aorta of SHR aged 13-14 months than in the aorta of WK rats. 4. It was supposed that kidney renin activity and lysosomal enzyme activities were related to hypertensive vascular lesions.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Vascular lesions in hypertensive rats under salt loading: kidney renin and lysosomal enzymes. 107 69

Dense gels of E. coli 70 S ribosomes, their 50 S subunits, CM-like particles, RNP strands and their fragments, 38 S particles obtained from RNP strand folding upon addition of Mg2+ ions, and of unoriented salt-free and free rRNA sodium and magnesium salts were studied by X-ray diffraction. It was shown that under dense gel conditions RNA molecules contained in ribosomes unfolded by desalting, like all other particles considered here, have helical regions. Under these conditions free desalted RNA has no helical regions. Experimental data on X-ray scattering at medium angles were compared with the diffraction curves calculated for homogeneous prolate and oblate ellipsoids, for various ellipsoids containing a dense region or an internal cavity, and for ellipsoids containing internal periodic regions. The results indicate that the internal structure of the 50 S ribosome is periodic, i. e., its components form a periodic lattice. The lattice spacings are approximately 42 and 28 A with a 0.8g/g dry weight sample water content. When the 50 S particle water content drops below 0.2 g/g dry weight the periodic structure is disrupted. This disruption is reversible. It was shown that CM-like particles at high ionic strenght (2 M LiCl) have approximately the same internal periodicity as the 50 S particles, but in contrast they lose this periodicity at low ionic strength (10-2M tris-HCl and 5-10-3 M MgCl2).
Mol Biol 1975 Jan
PMID:An x-ray diffraction study of ribosome structure. 109 99

1. 24 h aldosterone secretion rates (ASR) have been measured in six normal volunteers while recumbent all day and while standing for 12 h, on 200 and 10 mmol/day sodium diets and after salt-poor albumin infusions (75 g in 150 ml), which significantly expanded plasma volume. 2. The mean ASR on the 10 mmol/day sodium diet, both without and with the salt-poor albumin infusion, was highly significantly increased above the mean ASR on the 200 mmol/day sodium diet, both in the recumbent and in the upright posture. 3. There was no significant difference between the mean ASR values on the 10 mmol/day sodium diet alone and after the infusion of albumin either in the recumbent or in the upright posture. 4. The above abservations su;gest that sodium deprivation raises ASR by a mechanism or mechanisms unrelated to plasma volume.
Clin Sci Mol Med 1975 Mar
PMID:The role of plasma volume in the increase of aldosterone secretion rate during sodium deprivation. 111 36

1. Seven normal volunteers took 0-28--0-42 mmol (100--150 mg) of deoxycholate by mouth. This resulted in a reduced proportion of chenodeoxycholate in bile and an increased proportion of deoxycholate. Cholate was unchanged. 2. Cholate and chenodeoxycholate pools and rats of synthesis were determined in four of the subjects by simultaneously labelling each pool with 14C-labelled bile acids. The chenodeoxycholate pool and rate of synthesis decreased after deoxycholate administration. Cholate synthesis and pool size did not change appreciably. 3. The proportion of deoxycholate in bile samples of sixty-two subjects with intact enterohepatic circulation was found to be inversely related to the proportion of chenodeoxycholate in bile, but not to the cholate. 4. It is suggested that inhibition of chenodeoxycholate synthesis by deoxycholate, the principal bacterial product of cholate, regulates the size of the chenodeoxycholate pool independently of the total amount of bile salt.
Clin Sci Mol Med 1975 Apr
PMID:The selective inhibition of chenodeoxycholate synthesis by cholate metabolites in man. 112 22


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