Biomedical subjects

Brandon A Kemp

Publications and source records attributed to Brandon A Kemp.

6 recordsLinked to original sources

PubMed2006

Intrarenal aminopeptidase N inhibition augments natriuretic responses to angiotensin III in angiotensin type 1 receptor-blocked rats.

The renal angiotensin angiotensin type 2 receptor has been shown to mediate natriuresis, and angiotensin III, not angiotensin II, may be the preferential angiotensin type 2 receptor activator of this response. Angiotensin III is metabolized to angiotensin IV by aminopeptidase N. The present study hypothesizes that inhibition of aminopeptidase N will augment natriuretic responses to intrarenal angiotensin III in angiotension type 1 receptor-blocked rats. Rats received systemic candesartan for 24 hours before the experiment. After a 1-hour control, cumulative renal interstitial infusion of angiotensin III at 3.5, 7, 14, and 28 nmol/kg per minute (each dose for 30 minutes) or angiotensin III combined with aminopeptidase N inhibitor PC-18 was administered into 1 kidney. The contralateral control kidney received renal interstitial infusion of vehicle. In kidneys infused with angiotensin III alone, renal sodium excretion rate increased from 0.05+/-0.01 micromol/min in stepwise fashion to 0.11+/-0.01 micromol/min at 28 nmol/kg per minute of angiotensin III (overall ANOVA F=3.68; P<0.01). In angiotensin III combined with PC-18, the renal sodium excretion rate increased from 0.05+/-0.01 to 0.32+/-0.08 mumol/min at 28 nmol/kg per minute of angiotensin III (overall ANOVA F=6.2; P<0.001). The addition of intrarenal PD-123319, an angiotensin type 2 receptor antagonist, to renal interstitial angiotensin III plus PC-18 inhibited the natriuretic response. Mean arterial blood pressure and renal sodium excretion rate from control kidneys were unchanged by angiotensin III +/- PC-18 + PD-123319. Angiotensin III plus PC-18 induced a greater natriuretic response than Ang III alone (overall ANOVA F=16.9; P=0.0001). Aminopeptidase N inhibition augmented the natriuretic response to angiotensin III, suggesting that angiotensin III is a major agonist of angiotensin type 2 receptor-induced natriuresis.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2006

Intrarenal dopamine D1-like receptor stimulation induces natriuresis via an angiotensin type-2 receptor mechanism.

We explored the effects of direct renal interstitial stimulation of dopamine D(1)-like receptors with fenoldopam, a selective D(1)-like receptor agonist, on renal sodium excretion and angiotensin type-2 (AT(2)) receptor expression and cellular distribution in rats on a high-sodium intake. In contrast to vehicle-infused rats, sodium excretion increased in fenoldopam-infused rats during each of three 1-hour experimental periods (<0.001). Blood pressure was unaffected by vehicle or fenoldopam. In plasma membranes of renal cortical cells, fenoldopam increased D(1) receptor expression by 38% (P<0.05) and AT(2) receptor expression by 69% (P<0.01). In plasma membranes of renal proximal tubule cells, fenoldopam increased AT(2) receptor expression by 108% (P<0.01). In outer apical membranes of proximal tubule cells, fenoldopam increased AT(2) receptor expression by 59% (P<0.01). No significant change in total AT(2) receptor protein expression was detectable in response to fenoldopam. Fenoldopam-induced natriuresis was abolished when either PD-123319, a specific AT(2) receptor antagonist, or SCH-23390, a potent D(1)-like receptor antagonist, was coinfused with F (P<0.001). In summary, direct renal D(1)-like receptor activation increased urinary sodium excretion and the plasma membrane expression of AT(2) receptors in renal cortical and proximal tubule cells. D(1)-like receptor-induced natriuresis was abolished by intrarenal AT(2) receptor inhibition. These findings suggest that dopaminergic regulation of sodium excretion involves recruitment of AT(2) receptors to the outer plasma membranes of renal proximal tubule cells and that dopamine-induced natriuresis requires AT(2) receptor activation.

Anesthesia↗

PubMed2006

Passive guiding and sorting of small particles with optical binding forces.

We demonstrate the possibility of serially guiding and sorting nanometer-sized particles without the use of any external control. The working principle is based on an equilibrium between scattering and binding forces, the latter depending on the properties of the particles. A configuration is proposed that utilizes this property and is shown to efficiently sort small particles as function of their size.

Journal Article↗

PubMed2006

Optical momentum transfer to absorbing mie particles.

The momentum transfer to absorbing particles is derived from the Lorentz force density without prior assumption of the momentum of light in media. We develop a view of momentum conservation rooted in the stress tensor formalism that is based on the separation of momentum contributions to bound and free currents and charges consistent with the Lorentz force density. This is in contrast with the usual separation of material and field contributions. The theory is applied to predict a decrease in optical momentum transfer to Mie particles due to absorption, which contrasts the common intuition based on the scattering and absorption by Rayleigh particles.

Journal Article↗

PubMed2006

Stable optical trapping based on optical binding forces.

Various trapping configurations have been realized so far, either based on the scattering force or the gradient force. In this Letter, we propose a new trapping regime based on the equilibrium between a scattering force and optical binding forces only. The trap is realized from the interaction between a single plane wave and a series of fixed small particles, and is efficient at trapping multiple free particles. The effects are demonstrated analytically upon computing the exact scattering from a collection of cylindrical particles and calculating the Lorentz force on each free particle via the Maxwell stress tensor.

Journal Article↗

PubMed2006

Trapping and binding of an arbitrary number of cylindrical particles in an in-plane electromagnetic field.

The Mie theory and the Foldy-Lax multiple-scattering equations are applied to compute the scattered field of an arbitrary number of infinite dielectric cylinders of arbitrary size, subject to in-plane incidences. The Maxwell stress tensor is then used to compute the force on each cylinder. Trapping and binding forces are studied as a function of particle size, number, permittivity, and separation. Finally, the formulation is applied to a system of 20 particles, and the results show clear similarities with known experimental reports. The formulation presented here extends the capabilities of modeling particle interaction and optical matter beyond the simple cases of the Rayleigh regime and two-particle systems.

Journal Article↗