Adhesion of carboxylate cements to hydroxyapatite. I. The effect of the structure of aliphatic carboxylates on their uptake by hydroxyapatite.
An investigation was made into the effect of the structure and functionality of aliphatic carboxylates on their sorption onto hydroxyapatite with a view to ascertaining factors affecting the adhesion of polyacrylate cements to tooth materials. In general, the amount of carboxylate sorbed was found to increase with the number of groups contained in the molecule. Thus, polyacrylate was found to be much more strongly sorbed than low molecular weight species. Sorption of the low molecular weight species appeared to be related to stereochemical factors rather than to the stability constants of their calcium chelates.
Adhesion of carboxylate cements to hydroxyapatite. III. Adsorption of poly(alkenoic acids).
Investigations into the effects of relative molecular mass (RMM) and structure of poly(alkenoic acid)s on their adsorption on to hydroxyapatite (HAP) were carried out with a view to establishing factors that influence the adhesion of glass-poly(alkenoic acid) cements to tooth material. The effects of pH and fluoride addition were also studied. It was found that high adsorption levels were achieved under conditions of high chain entanglement, such as in a concentrated solution of a polyacid of high RMM. Theories of adsorption of carboxylic acids on to HAP are reviewed in the light of these studies and previous work at our laboratory.
The bradykinin B1 receptor and the central regulation of blood pressure in spontaneously hypertensive rats
We evaluated if the brain bradykinin (BK) B1 receptor is involved in the regulation of blood pressure (BP) in conscious rats. Basal mean BP and HR were 115±2 and 165±3 mmHg and 345±10 and 410±14 beats min−1 in Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR), respectively. Intracerebroventricular (i.c.v.) injection of 1 nmol B1 receptor agonist Lys‐desArg9‐BK significantly increased the BP of WKY and SHR by 7±1 and 19±2 mmHg, respectively. One nmol Sar[D‐Phe8]‐desArg9‐BK, a kininase‐resistant B1 agonist, increased the BP of WKY and SHR by 19±2 and 17±2 mmHg, respectively and reduced HR in both strains. I.c.v. injection of 0.01 nmol B1 antagonists, LysLeu8‐desArg9‐BK or AcLys[D‐βNal7,Ile8]‐desArg9‐BK (R715), significantly decreased mean BP in SHR (by 9±2 mmHg the former and 14±3 mmHg the latter compound), but not in WKY. In SHR, the BP response to R715 was associated to tachycardia. I.c.v. Captopril, a kininase inhibitor, increased the BP of SHR, this response being partially prevented by i.c.v. R715 and reversed into a vasodepressor effect by R715 in combination with the B2 antagonist Icatibant. I.c.v. antisense oligodeoxynucleotides (ODNs) targeted to the B1 receptor mRNA decreased BP in SHR, but not in WKY. HR was not altered in either strain. Distribution of fluorescein‐conjugated ODNs was detected in brain areas surrounding cerebral ventricles. Our results indicate that the brain B1 receptor participates in the regulation of BP. Activation of the B1 receptor by kinin metabolites could participate in the pathogenesis of hypertension in SHR.