Pubic Debt and U.S. Saving: A New Test of the Neutrality Hypothesis

The substantial post war decline in the U.S. saving rate has added great impetus to the debate over whether public debt policy crowds out saving. Rather than attempting to reject specific saving models, empirical research on debt policy and savings has primarily focused on the impact of particular policy variables on savings. In this paper we examine Barro's infinite horizon, intergenerationally altruistic model. A distinguishing feature of this modelis that aggregate consumption depends only on collective resources and not the age distribution of resources.To test this proposition we specify the Barro model under earnings uncertainty, rate of return uncertainty, and demographic change and test whether, given the level of consumption predicted by this model, variables measuring the age distribution of resources influence actual consumption. Data on the age distribution of resources are primarily obtained from the annual Current Population Surveys. Our results imply a rejection of the hypothesis that aggregate consumption is independent of the age distribution of resources.They therefore cast doubt on the contention that government debt policy does not affect consumption and saving.

Changes in the Age Distribution of Income in the United States, 1968-1984

Among the interesting changes in the U.S. economy in recent years have been the substantial changes in the age distribution of income and its components. These changes are interesting in and of themselves, but also are an important background against which to interpret aggregate economic statistics. In this paper we present detailed data on both the shares of income, and the relative income per household, of households headed by persons of different ages. These data are supplemented by analogous data for the various components of income: earnings, property income, Social Security, unemployment insurance, welfare, and pensions. These data are tabulated from 17 years of the annual Current Population Surveys (CPS). Among the most interesting trends are the dramatic increase in the share of income received by households over the age of 65 and also in their relative incomes; the enormous growth in the absolute and relative contribution of Social Security income to the incomes of households 55-64, and 65 and over; the sharp decrease in the share of total earnings and of the relative earnings of these two most elderly cohorts; and swings in the shares of total income of the other age cohorts which reflect in part changes in the numbers of persons in households of different ages, e.g., due to the aging of the baby-boom generation.

Social Security: A Financial Appraisal Across and Within Generations

This paper computes the expected present value of Social Security retirement benefits and taxes for households of different marital circumstances, incomes, and age cohorts. Also computed are the net gain or loss from participation in the system and the expected internal rate of return it offers various participants. The paper calculates the marginal linkage between benefits and contributions, and also examines how the age of entry into the covered workforce affects the participant. All computations are made for the 1985 Social Security and income tax laws. The general results are that Social Security offers vastly different terms to households in different circumstances. The net gain or loss varies by $200,000 and the real internal rate of return on contributions ranges from negative numbers to 6.6% for households of different ages, income levels, and marital status. These differences are far greater than the widely debated distributional affects of relevant income tax alternatives. We also find that there is a great deal of variance in the marginal linkage of benefits and taxes with many households facing a situation where the present value of benefits increases from 0 to 30 cents per extra dollar of taxes paid.

Capsaicin-Induced Ca2+ Influx and Constriction of the Middle Meningeal Artery

Research in the past on transient receptor potential cation channel subfamily V member 1 (TRPV1) has been limited to mainly nervous tissue TRPV1 because of the channel’s role in pain perception. Here, we studied the potential role of TRPV1 in vascular smooth muscle. We have observed that capsaicin, a TRPV1 agonist, induced constriction of the middle meningeal artery (MMA). Our goal was to decipher the mechanism of capsaicin-induced constriction of the MMA. Arterial diameter measurements showed that constriction due to 100 nM capsaicin (65.4% ± 3.7, n=7) was significantly diminished in the presence of the voltage-dependent calcium channel (VDCC) blocker 100 µM diltiazem (43.1% ± 8.1, n=7). Capsaicin-induced constriction was not significantly altered in the presence of the sarco/endoplasmic reticulum calcium transport ATPase (SERCA) inhibitor 30 µM cyclopiazonic acid (63.7 ± 9.0%, n=5) compared to control arteries (58.4 ± 8.6%, n=5). The unaltered capsaicin-induced constriction of the MMA in the presence of a SERCA inhibitor suggests that calcium-induced calcium release does not contribute to the overall calcium influx mechanism within the smooth muscle cells of the MMA. The diminished capsaicin-induced constriction of the MMA in the presence of a VDCC blocker suggests that sodium entry through TRPV1 channels can possibly lead to the membrane potential depolarization and increased activity of VDCCs causing further calcium influx. Furthermore, since the capsaicin effect was not abolished by the blockage of VDCCs, our data suggest that calcium entry through TRPV1 is sufficient to cause approximately 65% of the total constriction of the MMA in response to activation of TRPV1

Stretch-induced Calcium Release in Smooth Muscle

Smooth muscle cells undergo substantial increases in length, passively stretching during increases in intraluminal pressure in vessels and hollow organs. Active contractile responses to counteract increased transmural pressure were first described almost a century ago (Bayliss, 1902) and several mechanisms have been advanced to explain this phenomenon. We report here that elongation of smooth muscle cells results in ryanodine receptor–mediated Ca2+ release in individual myocytes. Mechanical elongation of isolated, single urinary bladder myocytes to ∼120% of slack length (ΔL = 20) evoked Ca2+ release from intracellular stores in the form of single Ca2+ sparks and propagated Ca2+ waves. Ca2+ release was not due to calcium-induced calcium release, as release was observed in Ca2+-free extracellular solution and when free Ca2+ ions in the cytosol were strongly buffered to prevent increases in [Ca2+]i. Stretch-induced calcium release (SICR) was not affected by inhibition of InsP3R-mediated Ca2+ release, but was completely blocked by ryanodine. Release occurred in the absence of previously reported stretch-activated currents; however, SICR evoked calcium-activated chloride currents in the form of transient inward currents, suggesting a regulatory mechanism for the generation of spontaneous currents in smooth muscle. SICR was also observed in individual myocytes during stretch of intact urinary bladder smooth muscle segments. Thus, longitudinal stretch of smooth muscle cells induces Ca2+ release through gating of RYR. SICR may be an important component of the physiological response to increases in luminal pressure in smooth muscle tissues

Ca2+-Induced Ca2+ Release through Localized Ca2+ Uncaging in Smooth Muscle

Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR) occurs in smooth muscle as spontaneous SR Ca2+ release or Ca2+ sparks and, in some spiking tissues, as Ca2+ release that is triggered by the activation of sarcolemmal Ca2+ channels. Both processes display spatial localization in that release occurs at a higher frequency at specific subcellular regions. We have used two-photon flash photolysis (TPFP) of caged Ca2+ (DMNP-EDTA) in Fluo-4–loaded urinary bladder smooth muscle cells to determine the extent to which spatially localized increases in Ca2+ activate SR release and to further understand the molecular and biophysical processes underlying CICR. TPFP resulted in localized Ca2+ release in the form of Ca2+ sparks and Ca2+ waves that were distinguishable from increases in Ca2+ associated with Ca2+ uncaging, unequivocally demonstrating that Ca2+ release occurs subsequent to a localized rise in [Ca2+]i. TPFP-triggered Ca2+ release was not constrained to a few discharge regions but could be activated at all areas of the cell, with release usually occurring at or within several microns of the site of photolysis. As expected, the process of CICR was dominated by ryanodine receptor (RYR) activity, as ryanodine abolished individual Ca2+ sparks and evoked release with different threshold and kinetics in FKBP12.6-null cells. However, TPFP CICR was not completely inhibited by ryanodine; Ca2+ release with distinct kinetic features occurred with a higher TPFP threshold in the presence of ryanodine. This high threshold release was blocked by xestospongin C, and the pharmacological sensitivity and kinetics were consistent with CICR release at high local [Ca2+]i through inositol trisphosphate (InsP3) receptors (InsP3Rs). We conclude that CICR activated by localized Ca2+ release bears essential similarities to those observed by the activation of ICa (i.e., major dependence on the type 2 RYR), that the release is not spatially constrained to a few specific subcellular regions, and that Ca2+ release through InsP3R can occur at high local [Ca2+]i

RYR2 Proteins Contribute to the Formation of Ca2+ Sparks in Smooth Muscle

Calcium release through ryanodine receptors (RYR) activates calcium-dependent membrane conductances and plays an important role in excitation-contraction coupling in smooth muscle. The specific RYR isoforms associated with this release in smooth muscle, and the role of RYR-associated proteins such as FK506 binding proteins (FKBPs), has not been clearly established, however. FKBP12.6 proteins interact with RYR2 Ca2+ release channels and the absence of these proteins predictably alters the amplitude and kinetics of RYR2 unitary Ca2+ release events (Ca2+ sparks). To evaluate the role of specific RYR2 and FBKP12.6 proteins in Ca2+ release processes in smooth muscle, we compared spontaneous transient outward currents (STOCs), Ca2+ sparks, Ca2+-induced Ca2+ release, and Ca2+ waves in smooth muscle cells freshly isolated from wild-type, FKBP12.6−/−, and RYR3−/− mouse bladders. Consistent with a role of FKBP12.6 and RYR2 proteins in spontaneous Ca2+ sparks, we show that the frequency, amplitude, and kinetics of spontaneous, transient outward currents (STOCs) and spontaneous Ca2+ sparks are altered in FKBP12.6 deficient myocytes relative to wild-type and RYR3 null cells, which were not significantly different from each other. Ca2+ -induced Ca2+ release was similarly augmented in FKBP12.6−/−, but not in RYR3 null cells relative to wild-type. Finally, Ca2+ wave speed evoked by CICR was not different in RYR3 cells relative to control, indicating that these proteins are not necessary for normal Ca2+ wave propagation. The effect of FKBP12.6 deletion on the frequency, amplitude, and kinetics of spontaneous and evoked Ca2+ sparks in smooth muscle, and the finding of normal Ca2+ sparks and CICR in RYR3 null mice, indicate that Ca2+ release through RYR2 molecules contributes to the formation of spontaneous and evoked Ca2+ sparks, and associated STOCs, in smooth muscle