Theory of regular arrays of defects: The void lattice
Defects in crystals may form a regular array, rather than a random distribution. The lattice of voids produced in irradiated molybdenum is a remarkable example of this. We give a general method of calculating the energy per defect in the array which exploits the periodicity of the defect lattice. The existence of the void lattice depends on the elastic interaction between voids. The present approach can treat both arbitrarily anisotropic elastic continua and discrete lattices, and is readily extended to discuss the stability of the defect lattice. The results predict that a void lattice should occur in molybdenum, and compare a number of models for the void. Stability against shear of the void lattice is not discussed in the present paper. The ratio of the void lattice spacing to void radius predicted is 2.2 to 4.5 and is smaller than the value of about 10 observed. The results are in general agreement with the more approximate Malen-Bullough treatment.
Stability of helium-filled platelets in nickel
Abstract In order to explain the observed behaviour of helium platelets, which grow and then collapse into clusters of smaller aggregates, a theoretical model is developed to describe the total energy of a platelet. The model is based partly on the results of atomistic computer simulations. The variation of the total energy gives information regarding the platelet stability and is calculated in both a numerical and an analytical way. It is shown that small platelets are stable and that, once a critical radius is attained, the platelet becomes unstable and a transformation into a group of smaller aggregates takes place. The theoretical model can also explain the fact that two-dimensional helium aggregates are observed to be more stable in b.c.c. than in f.c.c. structures.
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.