Near-infrared diode laser spectroscopy of free radicals.
Spectroscopic results on the radicals HCSi, CCO, and FeC obtained by studying in detail energy level structures using 0.8 microm diode laser system are reported. Of these radicals, the CCO radical was investigated mainly using Fabry-Perot type diode lasers with inconvenient mode gaps in the early stage of our near-infrared diode laser spectroscopic study of free radicals, and on the other hand, the FeC and HCSi radicals were studied using an external cavity diode laser. For the FeC radical, which is an interesting radical composed of an iron atom having 3d electrons, information on spin-orbit interaction between the triplet electronic ground state and a low-lying singlet electronic excited state is reported somewhat in detail. For the HCSi and CCO radicals, spectral particularities produced by a Renner-Teller interaction and a spin-orbit interaction are described for their high-resolution spectroscopic interest.
Laser Spectroscopy of the CCO Radical in the 0.77-μm Region: Analysis of theÃ(020)κ3Π andÃ3Πi(001) States
The A(020)kappa3Pi-X3Sigma-(000) and A3Pii(001)-X3Sigma-(000) bands of the CCO radical have been investigated by laser spectroscopy with two types of tunable laser system. An analysis was made simultaneously for both the bands to establish line assignments and determine molecular constants for both the A(020) and A(001) states. A coupling constant between these two states was also determined by assuming the interaction to be of Fermi type.
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.