The chemical process accompanying the hydrogenation of fats I. Geometrical isomerization
Summary1. It has been shown for numerous examples that the catalytic hydrogenation of fats is accompanied by the cis-trans isomerization of the radicals of the unsaturated acids.2. A scheme is proposed which explains the mechanism of the isomerization through a process of the hydrogenation-dehydrogenation of the olefinic compounds.
Modern State of the Multiplet Theor of Heterogeneous Catalysis
Publisher Summary This chapter reviews the modern state of the multiplet theory of heterogeneous catalysis. The multiplet theory deals with numerical values of bond lengths and bond energies, as well as with the geometrical form of reacting molecules and the crystal lattices of catalysts. This allows definite results to be obtained for many reactions on an atomic level. This is how the multiplet theory differs from a number of other theories on catalysis. The theory of the structure of matter is based on both electronic theory and quantum mechanics—the basis for the multiplet theory. Bond lengths and energies represent a stable complex of electronic properties essential for catalysis. The multiplet theory proceeds from the premise that catalysis is a chemical phenomenon and that covalent bonds require catalytic activation.
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.